Substance Abuse Disorders-combined PDF

1. Scope of the Problem ​ Correlates of Substance Use: ○​ Risk behavior, violence, antisocial behavior, accidents, fatalities, suicide risk ○​ The more substance use then the more above things happen (everyone demographically) ​ DSM-IV Alcohol Dependence: ○​...

1. Scope of the Problem ​ Correlates of Substance Use: ○​ Risk behavior, violence, antisocial behavior, accidents, fatalities, suicide risk ○​ The more substance use then the more above things happen (everyone demographically) ​ DSM-IV Alcohol Dependence: ○​ Lifetime prevalence: 13% ​ An underestimate bc ppl who have these problems are missed in these pop based studies such as incarcerated and homeless ppl ​ Comorbidity: ○​ Common with anxiety, mood disorders, schizophrenia, personality disorders (Anti Social) ○​ NUMBER ONE is another substance use disorder!! So it could be alcohol use disorder AND cocaine use disorder ​ Cost of Alcohol: ○​ Estimated $185 billion annually ○​ 3rd largest risk factor for disability & disease 2. DSM-5 Substance Use Disorders ​ Essential Features: ○​ Cognitive, behavioral, & physiological symptoms indicating continued use despite significant substance-related problems ​ Has biopsychosocial model built in! ​ There's a widespread recognition of a cognitive perspective in this disorder 3. Understanding Alcohol ​ Definition: ○​ Ethanol (ethyl alcohol) ○​ CNS depressant ​ Called sedatives or tranquilizers bc they diminish effects listed below ​ Effects: ○​ Impacts environmental awareness, sensory responses, cognition, physiology, mood - can be interpreted pos bc ppl desire relaxing anxiety inhibiting effects of these drugs ○​ Lethargy and amnesia as well are effects ​ Risks: ○​ Tolerance, dependence, and cross-potentiation  ​ Cross-potentiation is the uniformity of the action of these drugs then compounding each other, one exacerbates the effects of the other, very dangerous! ​ Can be for drugs like xanax or ambien which have these exacerbating effects w out ppl knowing it! 4. DSM-5 Criteria for Alcohol Use Disorder ​ Criterion A: A problematic pattern of alcohol use leading to CSDI, manifested w/in 12 mos by at least 2 symptoms: ○​ Impaired Control (Grouping 1) (at least 2 within 12 months): ​ Using more than intended, failed attempts to quit, time spent on obtaining/using/recovery, cravings ○​ Social Impairment (Grouping 2): effects of use pattern that’s present ​ Role failures - recurrent, social issues, abandoning important activities ○​ Risky Use (Grouping 3): ​ Continued use despite physical/psychological problems, using in hazardous situations which are recurrent like driving under the influence ​ Similar to personality disorders, person is aware of neg effects of their habits but they do not stop ○​ Pharmacological (Grouping 4): ​ Tolerance - markedly diminished effect when using the same amt ​ Withdrawal - every diff drug has a diff withdrawal symptom - you have to evaluate each medication that person takes and its withdrawal symptom ​ Reflect: Crazy you only need to hit 2 symptoms!!!! Very low bar (complication 1)!!! That means if you have 2 symptoms you’d be diagnosed w the same disorder as someone who has 11 out of 12, but they’re veryyyyy different ppl!!! Diagnosis is not synonymous w addiction (complication 2) 5. Genetic Factors in Alcohol Dependence ​ Heritability: ○​ Estimated 50-60%, especially high in early-onset males ​ Robert Cloninger's Study: ○​ Stockholm Adoption Study identifying traditional early onset and nontraditional late-onset drinking patterns ○​ Robert developed a study of a large birth cohort of children in Stockholm of kids who were separated from their biological parents and reared in homes of relatives who would adpot them ○​ He had extensive data on both parents of everything which helped study to see what are independent contributions of genes and the environment ○​ He determined 2 genetic based drinking patterns ​ Type 2 Alcoholics: Early and heavily - movies type  ​ Type 1:Alcoholics: Long periods w out drinking but then uncontrollable when they started drinking - non traditional ​ Diff b/w pattern is best explained by personality traits they could measure in childhood at 10 yo ​ Personality Influences: ○​ Traits like harm avoidance, novelty seeking, antisocial tendencies 6. Types of Alcoholics (Cloninger's Typology) ​ Type 2: Early-onset steady drinkers, mostly male, strong hereditary influence, antisocial traits ○​ 7x higher risk if their father was an alcoholic! ○​ Family environment had no measurable effect, boys began drinking regardless if ppl around them drank or not ○​ Patterns are driven by personality traits! ​ Low levels of harm avoidance like shy or fearful or worrier or avoids risk ALONG WITH high levels of novelty seeking like ppl who wanna try new things or explore or they’re impulsive or easily bored ​ Under Sensitive reward system so they seek excitatory effects from alcohol COMBINED WITH an under sensitive punishment system - weakly influenced by neg outcomes ​ Overlap with antisocial traits and disorder ​ Type 1: Late-onset binge drinkers, both genders, heredity and environment influence, cycle of abstain-binge-guilt ○​ Both females and males raised in heavy drinking environment so they avoid drinking early in life bc they saw the devastation that comes with it ○​ So if they drink then some of them experience very high levels of guilt ​ This leads them to further drinking to suppress the guilt! It works bc alc suppresses anxiety and guilt ​ THIS IS OPERANT CONDITIONING - NEGATIVE REINFORCEMENT!!!!! ○​ Referred to as late onset binge drinkers ○​ Pattern is strongly influenced by hereditary environmental interaction ​ Both parts are required to be type 1 ○​ Personality trait profile is high levels of harm avoidance and high levels of guilt and anxiety. These people have an oversensitive punishment system which causes their problems 7. Alcohol Metabolism ​ Blood Brain Barrier: ○​ Endothelial cells are packed closely together and the sheath then restricts those chemicals from getting to the brain ○​ It blocks water soluble molecules  ○​ Capillary walls have glucose transmitters that carry energy ○​ So we need to know that psychoactive drugs are water soluble so that it can pass through this protective barrier like in renal tubular cells aka kidneys cannot take it out of system ○​ Then its picked up by liver cells and in the liver they are enzymatically bio transformed (enzymes are processing them) ○​ Metabolites are carried back to kidney which can then be excreted ​ Process of Enzymatic Transformation: ○​ Ethanol → Acetaldehyde → Acetic Acid → CO₂ + Water ○​ 95% of alc breakdown is done by these 2 enzymes: ​ Enzymes: Alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) ○​ Rate of metabolization process - a higher rate for alc then theoretically lowers the threshold for dependence ​ How easy it is to become dependent ​ If you drink slowly then your body can keep up and you won’t feel anything ​ But if your consumption rate outpaces your metabolization rate then your BP is rising which effects your brain which is then the intoxication feeling ​ BUTTTT this rate is different person to person, you might have to be faster than someone else in order to feel the effects ​ Women have less of these metabolizing enzymes! ○​ Women drink less and are dependent less ○​ But interestingly enough women are very quickly catching up to men in terms of levels of them being diagnosed with AUD! ​ 13% now vs 9% in the past! ​ Genetic Mechanisms: ○​ Variants like ALDH2*2, ADH1B2 lower alcohol dependence threshold ○​ ALDH2 codes for production of enzyme ○​ ALDH2*2 is associated with slower enzyme which means if u drink at any pace then the ALDH will make u feel the effects stronger ​ Could be the flushing response and the hangover response ​ This version of this gene is considered protective, seen to have lower rates of heavy drinking and alc dependence ​ But ppl who are homozygous for this gene produce none of this enzyme, only 5% of those then become heavy alcoholics ​ Highly prevalent in north eastern asian countries and middle eastern ○​ ADH1B gene and ADH1B2 is similarly protected - slower metabolism process, feel more effects of alcohol ​ Found to be associated with lower rates of alc dependence ○​ SOOOOO the risk of ADH1B*1 and ALDH2*1 is associated with less of the metabolism rate which is less of the effects ​ More and faster consumption of alc 8. Additional Mechanisms in Alcohol Dependence ​ Neurotransmitters: ○​ High endorphin response, serotonin deficiency ○​ Endorphins bind with dopamine receptors - alc releases these chemicals ​ Some ppl have a genetically based high endorphin response to alc which means they drink more ○​ Alc increases serotonin ​ We know mood can be genetically determined along with low serotonin which can make alc use be genetically based partly at least ​ Personality Traits: ○​ Novelty seeking, harm avoidance, anxiety, antisocial tendencies ​ Above are associated with patterns of dependence ​ Harm avoidance and anxiety is associated w type 1 ​ Novelty is associated w type 2 ​ All above are partially heritable 9. Nongenetic Parental Influences ​ Parental Modeling & Accessibility: ○​ Influences attitudes, cognitive expectancies towards substance use ​ Modeling affects use so if you see you parents doing those action it'll then make it more likely for you to do it too ​ If ppl use in excess, it can also be modeled ​ If use is in form of coping from problems, that’s also associated with higher levels of use in teens ​ Accessibility is also key - do you know who your kids are hanging out with and what they’re doing ​ Higher levels of monitoring is directly related to kids use of alc n drug USE and ABUSE ​ Low monitoring increases the likelihood of them hanging out w deviant peers ○​ Deviant peers are marginalized and accept others who are also rejected in life so it can feel very accepting to be a part of them ​ When the quality of relationship with parent is good leads to less drugs and alc use ​ If parents hold positive attitudes towards drinking and drug use then it’ll influence kids expectancies with drug and alc use ​ Highest expectancies show highest dependency on alc and drug 10. Factors in Substance Use Maintenance & Escalation ​ Positive Reinforcement:  ○​ Pleasure stimulation (mesolimbic dopamine pathway), social acceptance ​ It's not known how alc increases meso dop pathway ​ Might be from release of indogenous opioids ​ Negative Reinforcement: ○​ Tension reduction, self-medication ​ Ppl use drugs and alc to cope with stress and it works in the short term ​ Reduction of an aversive experience is strongly neg reinforcing for any behavior ​ Dependence - body relies on the substance to function and without the substance then the body begins to rebel ​ They need the drug to avoid withdrawal and the symptoms of withdrawal can be mild to severe ○​ Can be with therapeutic drugs as well like SSRI’s if you stop suddenly ​ Tolerance: ○​ Decreased effect with repeated doses (metabolic, pharmacodynamic, behavioral conditioning) ​ Type 1: Metabolic ​ Presence of drug in liver induces synthesis of liver enzymes that are needed to process the drug ​ With repeated use, your enzymatic levels are increasing which will increase your levels of metabolization ​ Can increase from 50-70% which means your body has to drink more to get the same effects you’ve been getting!!! ​ Type 2: Pharmacodynamic ​ Neurons adapt to the continuous presence of a drug through downregulation ○​ Reduction in number or in drug sensitivity of neural receptors ​ More drug is needed bc u have fewer receptors ​ Type 3: Behavioral Conditioning ​ Saliva with CS → CR example ​ Cues that tell your body the drug is coming are associated with a counterintuitive process bc what they trigger is an effect that is opposite of the drug’s natural effect ○​ Morphine reduces pain sensitivity by activating opioid receptors. Brain protects this effect from being too strong by producing a compensatory effect. Brain knows excess release of those chemicals can kill you so it naturally compensates for that when it anticipates it coming. 11. Conditioning in Substance Use ​ Classical Conditioning:  ○​ Example with morphine: UCS (Morphine) → UCR (Pain Reduction) ​ Suppresses body’s natural expression of the drug ○​ CS (Injection Paraphernalia) → CR (INCREASE in Pain Sensitivity) ​ CR becomes different, a compensatory response ​ Increase in PS and increase in euphoria ​ But also more depressive respiratory response - neg effect ○​ They’re competing w each other so you consume more to deal with this effect ​ This is why OD happens more in novel environments ​ If environment is same then you will trigger the compensatory effect, but if it’s different env then the amt you use would be enough to kill you 12. Conceptual Model of Substance Use Disorder ​ Pathway: ○​ Exposure → Use → Escalation → Consequences & SUD ​ Influences: ○​ Social, cultural, psychological, biological factors ○​ Etiology of substance use disorder MODEL: ​ Central behavior for disorder - using the drug ALOT but the amts vary across individuals but not part of diagnosis for them ​ Many factors contribute to use of the drug ​ No one starts using in large quantities which means the critical behavior is escalating use - that's what we have to ultimately explain!!! ○​ End of lecture understanding: ​ All elements addressed in lecture ​ Culture is heavily built around alcohol ​ Drinking in excess or for celebrations - all cultural expectations in the USA ​ Different in france for example ​ Lots of potential factors within just culture! ​ Exposure to substances ​ Availability, peer use, modeling ​ Psych influences ​ Neg and pos reinforcement factors, cognitive effects like distortions ​ Stressors ​ Self medicating, using to cope, stress and use is bidirectional - reciprocal causality? ​ Biological influences ​ Sensitivity, metabolism, mood disorders!!! Anxiety disorders and personality traits  ​ ALLLLL amalgamate into feeding of escalation process which leads to the consequences that happen when escalation becomes more than what you can handle ○​ SOOOO treatment has to focus on ALL of the items mentioned above within one’s life 1. General Treatment Issues ​ Recognizing America’s Drug Problem ○​ Problem Recognition: ​ Common issue: Denial ​ Fail to recognize they have a problem or the nature of their problem until their lives are destroyed ​ Particularly common to be in denial for SUD ○​ Unless they are mandated - that’s how some get treatment - leads to reluctance ​ Withdrawal Challenges: ​ Symptoms, detoxification, cravings, high-risk periods ○​ Discontinue use is the next step - high risk period of 18 months!!!! ​ Dominant approach is abstinence ​ In those 18 months you’ll have overpowering cravings and intense withdrawal and have ready access to the drugs itself ​ Soooooo relapse in this period is incredibly high ​ Bc of intense withdrawal they’ll go through detoxification in the hospital - but now insurance doesn’t cover it so now it’s very likely to do it on your own with very little support ​ Craving is characterized by emotional desire ​ Can me most intense emotion someone has ever had or will have ​ Overwhelming urge to obtain the drug and use the drug ​ Includes attentional focus - can’t think abt anything else ​ Euphoric memories - all the great times and great pleasure, but not the negative parts ○​ They wan’t to get back ​ Includes cognitive distortions - it won’t hurt if i do it again, it wasn’t that baddd ○​ Seeking Treatment: ​ Importance of personal motivation ​ Old thinking was you needed this first - hit rock bottom first and then we can help you, but this was in the past ​ New thinking is that we can help you create this  ​ Motivational interviewing - more like an intervention that came out of Roger’s humanistic perspective, an attempt to solve ambivalence (strong feelings in opposing views) ○​ Examines the indv needs, goals, life situations - all realistic and hard core situation you are in ○​ Not about giving advice ○​ Key to have empathy to develop self efficacy ​ Suuuuper expensive for treatment ​ Availability issues - some countries and areas just don’t have this as a thing 2. Psychopharmacological Treatment ​ Marketed as anti craving drugs even though there’s no meaning to that, all marketed to have to be combined with therapy ○​ They recognize that meds aren’t a magical pill ​ This is operant conditioning bc if you take this pill and do it with alc then you’ll be violently ill soooo this makes you not drink again to not feel those effects! ○​ Butttt you could simply go back to stop taking after 2 weeks instead, only works if ur super motivated ​ Aversive Treatment: ○​ Disulfiram (Antabuse): Prevents breakdown of acetaldehyde, causing unpleasant effects when drinking ​ Within minutes you’ll feel violently ill and will last for several hours ​ Dizziness sweating heart palps - very bad ○​ Research shows its not effective as a deterrent and non compliance rates are very high ​ Agonist Substitution: ○​ Take a drug that has similar chemical makeup to original drug of choice ​ It’ll have less negative effects instead ○​ Methadone: Mimics opioid effects to reduce cravings ​ Has sedative effects until you develop tolerance for it ​ Effects of it are slower and less intense so you don’t get high AS LONG AS you take the recommended dose lol ​ Curbs cravings for heroin with correct dose ​ But it is addictive! ​ With counseling it reduces heroin use and criminal activity ​ Antagonist Treatment: ○​ These drugs block the effects of the drug so no euphoria from taking this drug bc medication is preventing that from happening ○​ Naltrexone (ReVia, Vivitrol): Blocks opioid receptors ​ Used for heroin and alcohol bc it suppresses intoxication which theoretically reduces cravings ​ You must be highly motivated for this to work ​ Anti-Withdrawal:  ○​ Acamprosate (Campral): Reduces withdrawal symptoms ​ Anti craving drug bc it dulls withdrawal symptoms and reduces high from alc intoxication and reduces relapse frequency ​ This drug is not well understood, mechanism not clear ​ It mayyyy restore the balance of neurotransmitters but not sure… ​ It may help bc it reduces emotional discomfort ppl are feeling like sleep problems during those 18 months of high risk period ​ Not any better than a placebo lowk 3. Community-Based Approach ​ Alcoholics Anonymous (AA): ○​ Core Principles: ​ Disease model, powerlessness, spirituality, sex bias ​ Step 1 of this is admitting a powerlessness over alc ​ The words Spirituality or God or Him are in 7/12 steps ​ Sex bias - why not Goddess or just women in general ​ Social support, normalization, anonymity ​ Only first names are used and strict rules of confidentiality ○​ But zero use of this in actuality - not enforced rlly ​ Big and Primary value of this approach is SOCIAL SUPPORT ○​ Normalization to see that you’re not alone in this ○​ Genuine support from others and new relationships that are outside of the culture of drinking/drug use that they might be involved in ○​ Considerations: ​ Sex bias in membership, reliance on social support ​ Every group is very different and only as good as the people in it ○​ There’s no control or hierarchy, just huge variability ​ Harm Reduction Movement: ○​ Goal : Possible to modify the behavior of drug use to reduce the risks to public health as well as to safety ○​ Examples: Needle exchange, methadone maintenance, safe use campaigns, treatment as alternatives to incarceration, controlled use ​ US gov has aggressively not used it until biden harris administration implemented it in policy, nowww we’ll see ​ 2 ways in appraches: Fed gov representing the ppl treats drug users by imprisoning them and AA embraces the medical model that addiction is a biological disease ​ Very black and white thinking and this leads to only acceptable option is abstinence ○​ Advantages of Controlled Use: ​ Lifestyle changes, higher compliance, option to avoid AA  ​ Avoids the person having to make a complete lifestyle change (which would've happened under abstinence approach) ​ Makes this a more attractive option which leads to compliance rates being higher ​ Avoids the rigid demands of AA, not bad just rigid, problematic for SOME not all 4. Controlled Drinking (CD) ​ Sobell & Sobell (1978): ○​ Techniques: Problem-solving training, moderation skills, monitoring internal cues, simulated drinking practice ​ Trained in problem solving and how to drink differently ​ Use your body cues and listen to them to train them - in a bar lab to make conditions feel realistic ​ They found success in teaching severe abusers to drink in a limited way, but was not welcome in the US as they had huge problems with this ​ Many outside of the lab then used these methods successfully but then a 10yr study follow up found that 1/20 had stuck with it and the 19 went back to abusing alc ​ Whole thing was controversial and it basically all went to the ground to try and advocate for this method ​ Evidence Suggests: ○​ Abstinence programs works for SOME but they have high relapse rates ​ Their relapses are better off like they continue drinking but not at dangerous levels like they did before ○​ Teachable Controlled Drinking skills for problem drinkers - possible! But we can’t predict which ones will be successful ​ Not for people that are DEPENDENT for sureeee 5. Treatment Outcome Comparison ​ AA: difficult to study and randomized but it’s possible. Now these findings are from controlled studies in last 15 years: ○​ Benefits: ​ Doubles abstinence rates (to ~40% in 1 year) ​ Comparing ppl who are doing this vs ppl who are not ○​ Ppl who are not are in treatment as usual but not AA ​ Improves motivation, commitment, coping skills, and self-efficacy ​ Mechanisms are unknown - we don’t know how they’re improving we just know they are ​ Research shows that it does improve those things above! ​ Remember it’s not a skill based program but it still works for that is very significant!  ​ Stable social support network ​ Very powerful for it to be genuine and stable!!! But no guarantee that it will fs ​ Spirituality can help certain people, just not all ○​ Challenges: ​ High dropout rate ​ 50% at 6 months will drop out of AA, 75% in 1 year ​ Not long enough for most ppl ​ But we don’t know the mechanism, we don’t know why ppl are dropping out ​ VERSUS Controlled Drinking (CD): ○​ As effective for moderate drinkers, comparable to abstinence outcomes ​ Neither are wildly effective at the end of the day 6. Relapse Prevention & Cognitive Behavioral Therapy (CBT) ​ Underlying dysfunctional psychological mechanism ○​ Faulty/maladaptive learning - bio mechanism ○​ faulty/maladaptive thinking - cognitive mechanism ​ Positive Expectancies & Abstinence Violation Effect: ○​ Addressing "slips" due to stress or situational demands ​ Distorted thinking and thoughts: “it wont be like that anymore! Im a different person now! I cant drink like before but trust i got this now!” ​ They truly believe this, not just projecting it ​ This is an “expectancy challenge” according to textbook ○​ Treatment is to challenge this expectancy AKA doing cognitive therapy - reengineer the way ppl think abt these issues, identifying these distortions and beliefs, showing them the evidence and help them to learn differently ​ “Slips” = failure of coping skills ​ Don’t think that one sip is just fuck it it doesn’t matter, it’s just a slip ​ Maybe stress got to you or wtv it was ​ Know that there’s places where risk is higher like going to parties ​ You need to learn skills like assertiveness and train them in it ​ You have to identify triggers for ppls cravings and make them alert that if that happens then this will then happen ○​ Teach skills to get out of those situations (COPE) once you’re alr in them without using the drug ​ High-Risk Situations & Coping Strategies: ○​ Developing problem-solving training, managing cravings ​ CBT Outcomes: ○​ Reduces positive expectancies around drinking, increases self-efficacy, reduces drinking behaviors  ​ Very important to increase self-efficacy - they’ll have confidence to go forward and face these situations head-on 7. Alternative Community-Based Approaches - NOT ON EXAM ​ Examples: ○​ Rational Recovery (RR), Self-Management & Recovery Training (SMART), Moderation Management (MM), Moderatedrinking.com (MD) ​ Resource: ○​ SAMHSA’s National Helpline: 1-800-662-HELP (4357) 1. The Challenge of Clinical Work with Children ​ Key Issues: ○​ Greater complexity of cases ​ May age out of certain problems ○​ Larger number of disorders ​ Children exp everything adults do in terms of disorders (other than personality disorder) ○​ Less research available ○​ Need for specialized training ​ Anyone can be an LPC and treat children 2. Assessment Issues ​ Limitations of Self-Reports - Validity Limited: ○​ Affected by developmental level ​ They don’t have that level of understanding or vocabulary to explain experiences ​ Parents are good reporters of behavior but not their (child’s) own experiences like self esteem ​ Child then ends up feeling upset bc of this and parent sees the child as angry and oppositional ​ You NEED perspective of any one that has knowledge like teachers, peers, siblings - secondary reporters ○​ Insight is limited ​ Ask them why are you here - you’ll have wild attributions ​ Oh my parents are getting a divorce so therapy for me is step one ​ Oh my parents are done with me so now you have to discipline me ○​ Motivation ​ They may not understand how they feel or why they did what they did ​ Importance of Multi-Mode Assessment ○​ Multiple reporters, bring all tools together ​ Critical Diagnostic Process: ○​ Many disorders begin in childhood (50% by age 14) ○​ Only 20% identified and treated ○​ Disorders interfere with normal development and may cause neurobiological impairments ​ Over half of children diagnosed with MDD will have symptoms for over 2 years! ​ Social withdrawal, academic failure ​ Even if they recover, they will be behind developmentally ​ Toxic levels of cortisol damage neural tissue or can interfere with brain development for children  ​ DSM Limitations for Children: ○​ Lacks sensitivity to childhood differences: ​ OCD: Compulsive behavior goals differ ​ SAD: fear may be expressed differently in children vs adults and they add a requirement that anxiety also happens in peer settings not just around adults ​ PTSD: intrusion expressed differently like in dreams and a separate criteria for under 6 yo ​ No change for duration ​ Feeling of detachment is not a symptom for children according to DSM ​ Child specific sub type for PTSD ○​ Only for preschool children ○​ Distress is not required for exp intrusion ○​ Only 1 symptom is required in 2 of major categories - avoidance & cognition and mood categories ​ PDD: only for 1 year (lowering of threshold) ​ NO MODS FOR: Bipolar, SUD, schizophrenia, ​ Joan Luby’s Modified Criteria for Preschool MDD: ○​ No duration requirement, age-appropriate manifestations of symptoms, validated through family history and social impairment ○​ They established construct validity of this type of criteria ​ Specific symptoms that were stable ​ Social impairment ​ Family history of mood disorders ○​ They found that 76% of children were not captured by normal criteria in DSM ​ Meaning that ⅔ of children have a meaningful mood disorder, but DSM fails to identify them! 3. Pediatric Bipolar Disorder (PBD) ​ Diagnosis: Same as adults ​ Prevalence: ○​ Rare reports before the 1990s ○​ 40x increase in office visits, 50% of hospitalizations under age 12 connected to diagnosis of BP ○​ Estimated prevalence for BP I: ~0.5% 4. Disruptive Mood Dysregulation Disorder (DMDD) ​ Criteria: ○​ “Severe” recurrent temper outbursts ​ Grossly out of proportion to situation  ​ But what does severe mean? Time/duration, volume, stronger emotional expression ​ Aren’t these all behavioral and can be operant conditioned? Environmental effect? ​ Inconsistent w/ developmental level ​ 3+ times weekly on avg ​ Mood b/w outbursts is persistently irritable (most, nearly every day) ​ Present for 12 or more months in at least 2 settings (“severe” in at least 1) ○​ Why is there no CSDI?? ​ It is definitely an impairment but it’s not included in DSM! 5. Childhood Major Depression ​ Epidemiology: ○​ Prevalence: ​ regulate emotion (frustration: “i dont wanna”-> self-talk (motivating to get shit done)-> reformulate (make a plan)-> act Treatment ​ Stimulant medication –​ Methylphenidate, amphetamine, & dextroamphetamine ​ Sometimes combined ​ Promote dopamine release ​ Last 4-12 hrs, feel it after 30 minutes –​ mechanism: improve dopamine efficiency ​ Inhibiting reuptake inhibitors happens in frontal regions (which control inhibition) –​ 75-90% significant improvement (over age 5) ​ Only when medication is in the symptom ​ sustained attention ​ impulse control ​ reduction of task-irrelevant behavior ​ productivity –​ Secondary benefits: ​ disruptiveness, noncompliance, aggression, academics –​ Doesn’t help success long term and larger projects/exams b/c they depend on skills that were missed developmentally ​ Stimulant side effects: –​ insomnia, appetite suppression, growth suppression –​ Rebound effect: irritability, hyperactivity, stomachaches, headaches ​ Not as common and get better with continual usage Reasons for other treatments ►​ Meds: 25% do not improve & 80% discontinue ►​ No evidence for long term effects or safety ►​ Removes incentive for other treatment ►​ Pervasiveness – secondary problems ►​ No effects: parenting, social relationships, academic ACH, severe comorbid behavior problems ►​ BT has “enormous” effects on ADHD symptoms AND significantly improves secondary problems! ❖​ BT+CMPT (contingency manage parent treatment?) should be frontline treatment –​ Should have parent operant conditioning training Changing Diagnostic Criteria ​ In the DSM 3 there were 6 mandatory criteria including ○​ “ a pervasive lack of responsiveness to other people “ ○​ “ gross deficits in language development “ ​ In the DSM 4 there are 16 optional criteria of which 8 are required ○​ Aspergers only required ⅔ of the half which would be 5 out of the 8 ○​ “ a lack of spontaneous seeking to share achievements with other people “ ○​ “ difficulty sustaining a conversation “ ​ The DSM’s language is critical, it was purposefully broadened, it clearly lowered the threshold which made it easier to diagnose the disorder Autism FACTS: ​ There is no autism epidemic ​ Autism is not caused by vaccinations ​ Facilitated communication is bogus ○​ Form of “treatment” developed for ppl with autism where a person holds the arm of the individual to allow them to type, thinking it was only a physical limitation not mental… Slide 1: DSM-5 Criteria for Autism Spectrum Disorder ​ A. Persistent deficits in social communication & social interaction: ○​ Persistent has no time period?? Not specific! ○​ Across multiple contexts, including: ​ Reciprocity ​ On a spectrum from “abnormal social approach and failure of normal back and forth conversations TO reduced sharing of interests of emotions of affect TO a failure to initiate to respond to social interactions” ​ Nonverbal communication ​ Relationship skills ​ B. Restricted, Repetitive Patterns of Behavior, Interests, or Activities: ○​ 2 out of 4 have to have deficits ​ C. Early Developmental Symptoms: ○​ Symptoms must be present during early developmental periods ​ “When is the early time period?? Is not specific” ​ D. Impairment: ○​ Must cause clinically significant impairment in functioning ​ Not distress bc the patient is not expected to have insight Slide 2: Epidemiology ​ Prevalence:  ○​ Autism Spectrum Disorder: 0.6%–2.2%, with dramatic increases over time ​ Demographic Effects: ○​ Sex: 3-4 times higher prevalence in males ○​ Socioeconomic Status (SES): Positive correlation ​ Universal disorder, seen across all populations Slide 3: Early Studies of ASD Course ​ Parental Report Studies (in the 70s that’s all we had): ○​ Observations of early developmental signs ○​ They reported many significant differences such as: Isolation, lack of play, lack of smiling, not cuddly, hypersensitive, treats me like an object, empty gaze, delayed speech ○​ This was not objective ​ Home Movie Method by Henry Massie: ​ Objective was to use parents home movie to be as objective as possible for children’s upbringing context ○​ 1st Year of child shows a lack of: ​ social smile, appropriate facial expressions, stable attention, and social interaction ○​ 2nd Year shows a lack of several new symptoms emerged including: ​ Ignoring people, preferring aloneness, lack of eye contact, gestures, and emotional expression ○​ Early Movement Disturbances: ​ Detected as early as 4-6 months, sometimes from birth ​ Delayed milestones such as sitting up, crawling, and walking ​ Reflexes may be “gone astray” Slide 4: 1st Birthday Party Observations ​ Key Indicators: ○​ Lack of looking at faces of others ​ More likely to stare into space or focusing on an object that’s irrelevant to social situation that was occurring ​ How often the babies looking at faces was the best single predictor of a later diagnosis of autism ○​ Limited joint attention: ​ Minimal pointing and showing behaviors ​ Conclusions ○​ Dysfunction in early social and cognitive development are DEVELOPMENTAL ​ Within the developmental process itself  ○​ Dysfunction involves “basic” brain systems Slide 5: Forms of Onset (Maestro et al., 1999) ​ Progressive Onset: ○​ Symptoms evident from first months of life, the course was slow and progressive ​ Usually around 3 months of age it’s evident ○​ Do not increase in vivacity or capacity for modulating affective states ​ Signs: Indifference, apathy, depressive moods, poor relationship development ​ Regressive Onset: ○​ Major breakthrough since it helped to explain the erroneous “cause” ○​ Typical early development with “free period” before onset even sometimes up to a full year ○​ Symptoms emerge between 12-18 months, a regression of their skill development: ​ Reduction in communicative gestures ​ Decreased interest in people ​ Lack of interest & response to speech ​ Fluctuating Onset: ○​ First months: Slight early delays in motor skills and hypo-reactivity to environmental stimuli ○​ At 6-18 months: communicative competence, improvement in interest - then it’s reduced ○​ 12 to 18 months: interact & imitate ○​ 18 to 24 months : symptoms appear clearly ​ Isolated, stereotyped play, loss of social competence Slide 6: Etiology: Prenatal and Perinatal Risk Factors ​ Environmental Risks: ○​ Exposure to toxins ○​ Medical conditions ​ Parental Factors: ○​ Paternal age ○​ Use of certain medications during pregnancy: ​ Valproic acid, SSRIs Slide 7: Biological Etiology  ​ Genetic Evidence: ○​ No single mutation explains a large number of cases ○​ Increased prevalence in siblings: ​ Broader autism phenotype: 4-20% ​ Significant cognitive deficits: 15-25% ​ Social interaction issues: 12% ○​ Concordance Rates: ​ Higher in monozygotic (MZ) twins than dizygotic (DZ) twins ​ Heritability estimated at 90% ○​ An autism gene??... NOPE Significant Risk Factors - some double the risk (still not very prevalent) ​ Identified prenatal & perinatal risk factors ○​ Urbanicty - more industrial and polluted w more toxins, the risk goes up accordingly ​ Mothers living near highways have 2x the risk of their child developing autism ○​ Maternal medical conditions - hypertension and obesity ​ They increase the risk and is believed to be a function of a disrupted immune system which affects the fetus ○​ Obstetric complications - like breach and fetal stress are risk factors ○​ Parental age - being over the age of 40 is a risk factor for mothers and over 50 for fathers ○​ Medication - valproic acid is an anticonvulsant to treat bipolar disorder ​ Potential risk factor is acetaminophen (tylenol) - not fully proved and studied but its getting there Slide 8: Etiological Mechanisms ​ Neuropsychological Factors: ○​ Deficits in attention, memory, language, and executive function ​ Distributed brain system not structure ​ Large variability ○​ Social information processing - greater consistency vs just processing info generally ​ In a 2 yo brain, the electrical patterns when being shown objects vs faces are very different ​ With autism the difference may not be there at all ​ Shows us its specialized in social cognition ​ Neuroanatomical Factors: ○​ Brain size/growth abnormalities  ​Theory: autism is caused by abnormal cell growth ​White matter volume < norm ​Gray matter volume > norm ​At age 2-3 its 10% larger and the rate of development slows down by adolescence and then they’re only 2-3% larger ​ Temporal and frontal lobes show little growth between age 2 and 6 ○​ Increase cell density in these brain structures ○​ Key brain areas: hippocampus, amygdala, cerebellum (Purkinje cells) ​ Cerebellum is underdeveloped ​ Children are clumsy and uncoordinated ​ It releases GABA ​ Purkinje cells are at a loss within the brain ​ Neuroimaging Findings: ○​ Altered activity in the prefrontal and parietal cortex Slide 9: Treatment: Applied Behavior Analysis (ABA) ​ Overview: ○​ Developed by Ole Ivar Løvaas ​ Single empirically reviewed treatment for autism ○​ Based on operant conditioning principles ​ Targets: ○​ Language/communication skills ○​ Social skills ○​ Self-care and adaptive behaviors Slide 10: Treatment: Early Start Denver Model (ESDM) ​ Developed by: ○​ Sally Rogers and Geraldine Dawson ○​ Typically a 2 year program ​ Focus: ○​ Parent-child interaction to strengthen social, language, and brain systems ​ Key Strategies: ○​ Facilitate early social attention, engagement, and reciprocity ​ Implemented in a naturalistic and social context ​ Target age-appropriate behaviors and skills to focus on ​ Emphasize social engagement which is a motivator to participate and be able to learn from the therapist Slide 11: ESDM Outcomes ​ Significant Improvements: ○​ IQ (17% increase vs 10% with the control - HUGE NEWS), language, social, and adaptive behaviors ​ Brain Normalization: ○​ Normalized responses to social stimuli - cortical activation ○​ Changing the way the brain is functioning with behavior therapy!! Wild!! ○​ Controlled group of community intervention - they’re actually declining and not improving vs ESDM kids are improving ​ Diagnostic Impact: ○​ Change in diagnosis for some children from autism to a diagnosis of pervasive disorder not otherwise specified (pre DSM 5 era) ○​ Shows we see movement in level of severity Slide 1: The First Issue: Competence to Stand Trial ​ Key Criteria: ○​ Rational and factual understanding of legal proceedings ​ Ability to consult with an attorney with rational understanding ​ Focuses on the defendant’s current state of mind ​ during arraignment, or trial, and/or sentencing after trial is over ○​ Not during the crime itself ​ Judicial decision determines competence ​ Judicial decision - the court decides thru experts Slide 2: Andrea Yates’ Competence ​ Defense (Dr. Gerald Harris): ○​ Claimed hallucinations and delusions ○​ Denied mental illness ○​ Easily confused and manipulated ○​ Position: Incompetent ​ Prosecution (Dr. Steven Rubenzer): ○​ Identified depression, suspiciousness, and delusions ○​ Denied mental illness ○​ Desires punishment for herself ○​ Position: Competent Slide 3: Insanity Defense: Foundations ​ Legal Principles: ○​ Actus Reus: "Guilty act" – act of committing the crime ○​ Mens Rea: "Guilty mind" – intent to commit the crime ​ Awareness of the implications of the act and intention that those occur ​ Definition of Guilt: ○​ Guilt requires both an illegal act and intent → guilt = legal act + intent Slide 4: Insanity Defense Standards - define the deficit in judgement and cognition caused by a mental disorder ​ As a result of mental disease or defect… ; at the time of the act  ​ “It must be proved that at the time of committing the act, the accused was laboring under a defect of reason, caused by Mental Illness, so as not to know the nature of the act or that he was doing wrong.” ​ McNaughten Rule (1843): ○​ “I didn’t know what I was doing” or “I didn’t know what I was doing was wrong” ○​ 2 Part: Cognitive test and Moral test ​ Irresistible Impulse Test (1886): ○​ “I could not stop myself” ○​ Volitional Test Slide 5: Additional Insanity Defense Standards ​ Durham Test (1954): ○​ “My mental illness made me do it” ○​ Product Test ​ American Law Institute (ALI) Standard (1972): ○​ “I could not know it was wrong” or “I could not stop myself” ○​ Includes moral and volitional tests Slide 6: Current Federal Insanity Defense Standard (1984) ​ Criteria: ○​ “I could not know it was wrong” ○​ Defendant lacks the capacity to appreciate the wrongfulness of conduct due to mental disease or defect ​ Burden of Proof: ○​ Defense must present clear and convincing evidence Slide 7: Texas Insanity Defense Standard ​ Info: ○​ Defendant “did not know that the conduct constituting the crime was wrong” - definition ○​ Limited to severe mental illness cases ○​ No clarification on what “wrong” means (in texas its undefined) ​ Burden of Proof: ○​ Lies with the defense Slide 8: Andrea Yates’ Insanity Defense ​ Defense: ○​ Claimed Yates knew her acts were illegal but believed she was doing the right thing ○​ She was too sick to know her actions were wrong ​ Prosecution: ○​ Downplayed her mental illness history ○​ Argued that her actions were intentional and she was sane ​ Jury: ○​ Jury was “death qualified,” indicating a bias toward capital punishment ​ Verdict: ○​ Guilty, after only 40 mins of deliberation! ○​ But then it was later thrown out due to someone calling out the expert witnesses’ testimony that was found to have been incorrect. A retrial was then called. Slide 9: The Field of Forensic Psychology ​ Specialization: ○​ Clinical psychology focused on evaluations for adjudication ​ Roles in Criminal Justice: ○​ Criminal profiling ○​ Trial consultation (jury selection, case preparation) ​ Research Areas: ○​ Criminal behavior, lie detection, eyewitness testimony, and false confessions Slide 10: Resources in Forensic Psychology ​ Professional Organization: ○​ American Psychology-Law Society (AP-LS) ○​ Website: http://www.ap-ls.org 1. Historical Background ​ Emil Kraepelin: Introduced "dementia praecox" – emphasis on early onset and deteriorating course. ○​ Established conceptual framework for what is now known as schizophrenia - his greatest contribution ○​ All his work was based on observations of patients and their symptom course ○​ He subdivided ppl w psychosis into two groups - “manic-depression” and “dementia praecox” ​ Dementia praecox was more complicated than the first group ​ More cognitive which emphasized its more chronic and deteriorating course, no remission ​ “Praecox” highlights early onset in adolescence ○​ He came up w comprehensive description of praecox including hallucinations and delusions, but didn’t consider psychosis to be most important part ​ Reductions in speech coherence and interests were most important part of disorder ​ Cognition and emotion > perception ​ Eugen Bleuler: Distinguished fundamental vs. accessory symptoms; coined "schizophrenia" to reflect fragmented thinking. ○​ Wanted to clarify psychotic disorders by dividing symptoms into two broad categories ​ 1. Fundamental symptoms ​ Loss of ability to connect threads of ideas / coherence in thought process ○​ Bc ppl can’t do that, their thinking becomes illogical and bizarre ​ Emotional deterioration ○​ Limited or no emotion at all ​ Found to present in all cases and exclusive to psychotic disorders ​ *** pathognomonic!!!! *** ​ Not psychosis being most important, but the thought process! ​ 2. Accessory symptoms ​ Occurred in a variety of disorders ​ Abnormalities in perception and cognition ​ He disagreed w Kraeplin in his conclusion of chronicity and deterioration being inevitable ​ He then made a better name and chose schizophrenia! ○​ Did this to demonstrate the fragmented thinking it most important part of disorder ​ John Hughlings-Jackson: Focused on loss of functioning vs. emergence of aberrant experiences.  ○​ Neither Kraeplin or Bleuler used the terms positive and negative in regards to symptoms, but Jackson did ○​ His view was that some symptoms reflected a relatively pure erosion of abilities which was referred to as negative symptoms ○​ But other symptoms were emergence of something aberrant - new stuff happening which doesn't usually happen to other ppl ○​ He was first to address underlying neurological mechanisms ○​ First half of 20th century is when negative symptoms dominated, seen to be most debilitating and pathognomonic ​ Clinicians were taught to diagnose based on this loss of functioning ​ Butttt due to problems w reliability, this focus began to shift in the 60s 2. Evolution of Focus in Diagnosis ​ Early 20th Century: Emphasis on negative symptoms; diagnostic challenges. ​ Robert Spitzer (DSM III): Shifted focus to positive symptoms, de-emphasizing negative symptoms. ○​ Heavy interest in improving diagnostic precision and reliability ○​ emphasis on positive symptoms ​ Easy to define and rate reliably vs negative symptoms that don’t/can’t ​ Bc you need a cutoff for neg but not pos ○​ Dsm 3 now ignores neg symptoms ​ ⅗ were positive symptoms in nature and the 6th was thought incoherence 3. Symptoms of Schizophrenia ​ Positive Symptoms: ○​ Cognitive, perceptual, behavioral abnormalities (e.g., delusions, hallucinations, bizarre behavior). ○​ Using these terms (pos vs neg) have become accepted ○​ These symptoms fluctuate considerably and go into remission between episodes ○​ They are often effectively treated with medications ○​ Delusions - unshakable (despite being logically inconsistent) false idea or belief ​ Not attributable to educational, social, or cultural background (u can believe in santa lol) ​ Patterns is that most common content is persecution but also you see other themes like grandiosity, jealousy, religious, and influence/control ○​ Hallucinations - false perceptions that represent perception w out object (sitting in room and have perception that room is breathing and walls are moving - this would be an illusion VS if u see bugs on the walls then that would be hallucination) ​ 50% of patients exp audio hallucinations and 15% experience visual hallucinations and 5% experience tactile hallucinations  ​ auditory hallucination - most common are voices talking to the patient or talking to themselves, usually voices are critical of the patient in an extreme way but occasionally they’re nice voices ○​ reported as objective and clear and coming from the outside ○​ repeat the patients thoughts and comments on their actions ○​ Self relevant - about you, not like the weather ○​ Behaviors - not consistent with reality, bizarre, no reason for it to be happening ​ Taking off clothes in public, lining up apples on store of grocery store, wandering aimlessly, unusual mannerisms ​ Catatonic behavior - person becomes rigid and immobile, unresponsive and mute, potentially staring, they are conscious but behaving as if they are not ​ Negative Symptoms: ○​ Reduction/deficit in cognitions, emotions, or behaviors (e.g., avolition, alogia - reduction in amt of speech or content depth of speech like empty replies, anhedonia - loss of ability to exp joy, asocial behavior - severe withdrawal from social relationships, affective flattening - external display of emotion is now blunted like diminished facial expressions, apathy, amotoricity - psychomotor retardation like slowed speech and movement). ​ Correlated with severity and recovery ○​ Anyone can exp time to time but in these cases are extreme and durable ​ Thought Disorder: don’t quite fit into pos and neg scheme, they represent deficit end ○​ Characterized as disorganized speech ​ Fails to communicate meaning or conveys meaning which does not fit context ​ Irrelevant answers to questions - tangentiality ​ Shifting topics abruptly - loose associations ​ Severely disorganized - incomprehensible - word salad ○​ Other cognitive deficits ​ Attention deficit ​ Memory ​ Abstract thinking 4. DSM-5 Diagnostic Criteria A.​ Two or more of the following for one month, with at least one being a, b, or c: a.​ Delusions b.​ Hallucinations c.​ Disorganized speech d.​ Grossly disorganized/catatonic behavior e.​ Negative symptoms B.​ Functioning below level achieved prior to onset  C.​ Continuous signs persist for at least 6 months 5. Epidemiology ​ This disorder is labeled as a “universal human scourge” ​ Lifetime prevalence: 0.5-1%. ​ Comorbidity: High prevalence of substance use disorders (SUD) 31-80% and tobacco use. ○​ Direction of effect is not fully clear, but probably bidirectional ○​ Many ppl are self medicating ○​ We know substance use earlier in life can lead to early onset ○​ Marijuana is most commonly used ○​ Chronic marijuana abuse contributes to the risk of psychosis due to THC and dopamine transmission - found from longitudinal prospective studies ○​ Tobacco use is probably bidirectional to schizophrenia ​ Those who smoke have a 2x risk of developing schizophrenia later in life - longitudinal and prospective ​ Smoking more = more risk ​ Prenatal exposure to smoking is a risk factor for schizophrenia ​ Demographics: ○​ Onset typically in late adolescence/early adulthood ​ 20% of cases develop after the age of 40 ​ Early onset = worse course, progressive loss of cortical gray matter in the brain ○​ For men, it’s not more but rather they get it earlier and the course is much worse ​ Women is later onset and fewer symptoms and fewer hospitalizations ​ Estrogen hypothesis - estrogen has a protective effect, psychotic symptoms improve when estrogen levels are higher and worse when those levels are lower ​ Maybe women get it later and this gives them more time to get educated, more relationships and marriage time which leads to later onset and less severe ○​ SES - disorder impacts education early and this has effects in low SES ○​ Race & Ethnicity ​ Symptoms are equivalent across ethnic groups BUT black americans are 2x as likely to be diagnosed w schizophrenia vs white or latino americans ​ From biases of clinicians ○​ Higher familial rate of substance use disorders 6. Comprehensive Impairment ​ Social and Functional Impact: Affects relationships, self-care, often leads to reliance on family or homelessness. ○​ Negative emotions  ​ Schizoaffective disorder, anxiety, anger, depression ○​ SUD’s ​ Maybe motivation issues, substance use is form of self medication and we take that away from you ​ Insight - level of insight is undermined by SUD’s, lack of insight is a major problem - noncompliance with treatment ​ If you don’t address it, treatment might be undermined ○​ Impairments in Social Functioning ​ Very difficult to establish relationships and hard to maintain existing relationships ​ Working becomes very hard with the roles involved like being a student or a parent ​ Lack of hygiene contributes to undermining social relationships ○​ Problems in Daily Living ​ Self care ​ 40-60% live with relatives and even higher % depend on relatives to be functioning ​ If those relationships erode, you’re reliant on mental health systems just to survive ​ 20% of homeless population probably has schizophrenia 7. Premorbid Development ​ Early deficits in multiple domains ○​ Cognitive functioning ​ Lower IQ scores are seen as well as poorer grades when assessed in school ○​ Social functioning ​ They are less responsive in social situations, they show less emotion, and they show more negative facial expressions identified as early as 1 years old! ​ Suggests our earliest relationships are being affected by subtle manifestations of this disorder ○​ Motor functions ​ Deficits in early milestones such as walking and bimanual manipulation which is anything that requires 2 hands to work together like opening a bottle ○​ Deficits tend to persist but most parents don’t recognize there were irregularities that their children were mentally disturbed ○​ All of this changes in adolescence - recognizing distinct problems ​ Not as obvious - seen as depression, irritability, non compliance 8. Course of Schizophrenia  ​ Onset in adolescence or young adulthood; typically chronic with variable symptom patterns and severity. ○​ It can start very suddenly or gradually - lots of variability ○​ The condition is episodic ○​ Severity - ​ ⅓ patients have a relatively mild course - fewer psychotic episodes and less hospitalizations and may live independently w enough support ​ ⅓ have an intermediate course - more freq tenuous social functioning, more hospitalizations etc ​ ⅓ are on a debilitating course - most of time in hospitals, no social relationships etc ​ Economic impact: High personal and societal costs. ○​ 281.6 billion for societal costs ○​ Real cost is in ppl’s lives personally, it’s inestimable 9. Prognosis and Predictors of Outcome ​ It would be nice to be able to tell the course of the indv but we don’t have a good ability to do that ​ Poorer prognosis is associated with ○​ Being male ○​ Socially isolated (the more, the worse it is) ○​ Behavior problems (anti-social behavior) ○​ Negative symptoms - lowk might being ignored ○​ Positive history (runs in your family) ​ Maybe a strong genetic component leading to more severe disorder? ​ Symptom severity & functioning depends on the dynamic interaction of MANY factors! ○​ Treatment availability and compliance ​ Not very avail for many ppl and even when it is, ppl aren’t always compliant w treatment ○​ Substance abuse ​ Makes things much worse being dependent on a substance ○​ Hostile or critical environment ​ Very diff for these (schizo) ppl w limited brain capacity to be able to cope with ○​ Assertive case management ​ Most goes untreated, many are institutionalized either in prison or state hospital and within most of them - the care is suboptimal ​ Assertive case management approach has a stigma of it being veryyyy expensive, but it’s actually not compared to being institutionalized ​ Ppl need support and being proactive and bringing it to where the ppl are 10. Genetic Factors  ​ Heritability estimated at 83%; certain genes (e.g., COMT polymorphism) linked to increased risk. ○​ Genetic effects are believed to be the dominant distal cause!!! ​ 83%!! ○​ Children born to moms w schizophrenia show more symptoms vs children w schizo w out moms having it too ○​ High functioning family serves as a protector for severe schizo effects ​ All antipsychotic meds block dopamine ○​ Correlated w/ effectiveness* ○​ They vary in how much they affect other neurotransmitters ○​ DA antagonisms how they completely block dopamine differs xyz ​ COMT gene is noted as most noteworthy gene in schizophrenia ○​ 1/4000 births produces the 22q11.2 deletion syndrome ​ This syndrome is caused by the deletion of a small part of chromosome 22 ​ This means the individual is missing 30-40 genes - not good! ​ 10% of the time this is inherited but most of the time it’s a random error ​ Signs and symptoms of syndrome ​ Heart defects, facial abnormalities, learning problems, immune problems, ADHD and Autism ​ Deletion leads to infant only having 1 copy (instead of 2) and codes for breaking down DA (catechol-o-methyltransferase) ​ Not able to efficiently break down DA leading to excess DA in the brain ​ 30% who have this syndrome are diagnosed with a psychotic disorder ​ COMT polymorphism (Val Allele) leads to reduced enzymatic activity ​ Genetic predisposition more pronounced in high-stress family environments. 11. Prenatal and Perinatal Influences ​ Seasonal Risk Factors: ○​ Higher risk in winter births due to potential viral infections ​ One of the strongest non genetic risk factors for the development of these disorders ​ 5-8% higher - significant but not craaazy difference ​ Observed in the northern hemisphere and less in the southern hemisphere and equatorial regions have no difference ​ Seasonal Fluctuations: Nutrition, hormones, meteorological factors ​ Sunlight exposure, temp, severe weather ​ Orrrr seasonally mediated viral infections ​ Pregnancy/Birth Complications: ○​ Higher prevalence birth complications ​ 2x risk if exposed to pregnancy and birth complications  ​ Schizo patients have a higher incidence rate of preeclampsia, bleeding, diabetes, asphyxia, and emergency c-section ​ Dev fetus w any of the above can lead to their oxygen being compromised - hypoxia ​ Odds of dev schizo increase linearly the more the infants are exposed to the above events ○​ Maternal viral infections ​ Epidemiological research shows higher levels of schizo in infants born shortly after a flu epidemic - self report ​ Strongest line of research take blood samples and determine if virus is there or not ​ Suggest prenatally exposed - increase in factors but depends on what infection was seen ○​ Toxoplasmosis (2.6x), flu (3x), genital/reproductive infection (5x) ○​ Stressful experiences during pregnancy ​ These hormones can disturb fetal neural development ​ Noise, social isolation and pain → strong surge in hormones → permanent changes in brain including hippocampus → related to behavioral change ​ Changes in their ability to learn has also been documented ​ Higher rates of schizo in offspring of women whose spouse dies during pregnancy also w women exposed to military invasion during their pregnancy ○​ Suzanne King ​ The more the objective exposure to the natural disaster → the less the children’s cognitive performance was ​ Subjective stress & Maternal CORT levels → asymmetrical fingerprints ​ Asymmetrical fingerprints are related to some brain abnormalities ​ Each aspect of stress that was measured (objective, subjective and hormonal) was associated with an increased risk for schizophrenia ​ MEANSSSS try to limit stress!!! 12. Brain Impairment and Neurobiology ​ Structural: Reductions in gray and white matter consistent across patients, particularly in the frontal cortex and hippocampus. ○​ Enlarged ventricles in schizo twin - up to 130% greater size compared to controls ○​ Gray matter in brain is reduced widely, severely, and progressively ​ Differences in GM and WM is evident when the disorder ONSETS, not necessarily when it was diagnosed a problem was seen ​ Research shows continual decrease ​ Counterintuitively - the reductions are more pronounced among ppl who are taking antipsychotic medications!  ○​ Decreased brain volume ​ In temporal lobe, frontal brain, and the whole brain in general ​ Hippocampus volume is the most consistent differentiator with studying healthy vs schizo brains ○​ Reduction in HC is where you see most differences between monozygotic twins where one has disorder and the other doesn’t ​ Functional: Decreased frontal cortex activity; elevated dopamine receptor density. ○​ Fiber density diffusion allows us to see how effective the communication is within the white matter part of the brain ○​ Reduced activity in prefrontal cortex ​ Most dramatic difference when person is engaging in working memory tasks ​ It's proposed that working memory is the key dysfunctional psychological mechanism!!!! ○​ There’s an elevated DA receptor density ​ Increased release of dopamine in subcortical regions - primarily seen when person is actively psychotic ​ There’s also neg symptoms that have been found to be associated w DA reduction in prefrontal cortex ​ Soooo the earlier idea of its all abt DA is kinda not that simple - need to know what part of brain you’re talking abt ○​ NOT JUST DA!! There’s glutamate, GABA and acetylcholine are all related to schizophrenia as well ​ Research shows that those transmitters are more associated w neg vs pos symptoms 13. Treatment of Psychosis ​ Medications: ○​ Primary effect of antipsychotics is to reduce psychotic thought process (blocks DA to reduce those symptoms) ​ Less misinterpretation of information ​ Delusions and hallucinations become less likely and reduced ○​ Other / secondary effects include ​ Calming effects, reduce risk of psychotic relapse - prophylactic effect, greater benefit from psychosocial treatment - family therapy, it reduces the risk of suicide ​ About 20-40 drugs in this class that are on the market ​ Math suggests there’s more medications than schizo patients to take it LMAO sooooo how’d they solve this problem? ○​ Side effects of greatest concern: ​ In the short term  ​ Extrapyramidal symptoms - can take the form of Parkinsonism and Akathisia which is when they can’t stand still and they’re always moving (Parkinsonism - physical calming but more like straitjacket form of calming lol) ​ In the long term ​ Tardive dyskinesia (involuntary movement of the muscles most commonly in lips and tongue) ​ Adverse metabolic effects ○​ Weight gain and diabetes ​ Other effects in as much as 50% of cases ○​ Toooo many effects lmao ​ Optimal Approach: Combination of medication and psychosocial interventions - 60% of the time these drugs are left w persistent neg and pos symptoms in ppl!! Even when they’re med compliant!! ○​ Family Psychoeducation Therapy: ​ Improves family members knowledge and coping ​ Reduces relapse and hospitalization ○​ Assertive Community Treatment: ​ Reduces time spent in hospitals, stabilizes housing, increases patient and family satisfaction ​ The team delivers treatment where and when needed - on the road ○​ Social Skills Training: ​ Improves social competence and compliance ○​ CBT: ​ Reduces symptom severity by addressing negative thought patterns. 14. CBT for Schizophrenia (ABCs Model) ​ Focus on changing beliefs that drive negative emotions, leading to improved mental health outcomes.