Therapies, Treatments, and Exam Overview

Alright guys, let's get started. Okay, wrap up your conversations. It's the last lecture before the final. So, we'll wrap up chapter 17, we'll do our little review game, and then we'll leave the remaining time for any questions that you have about any of the content in the course. How many of you got a chance to see the eclipse, by the way, yesterday? Not very many. Even from here, it's still pretty cool. Okay, one thing I forgot to mention last class. So we were talking about the efficacy of the different types of therapy, and how there are big meta-analyses indicating that there's probably not that big of a difference between the different types. But I forgot to mention there was another meta-analysis that compared specifically CBT, which is probably the most commonly used, it's a cognitive behavioral therapy, it compared that with generic counseling. Which is closer to a good placebo, right? Just general counseling without any specific therapeutic strategy. And that meta-analysis had over 30,000 people and it was found that there was an advantage for CBT. They defined recovery as your depression score declining by a certain number of points. And when you... use that definition, 60% of people who were undergoing CBT recovered, whereas only 40% in the generic counseling conditions recovered. Now, this advantage only became... significant after about 18 weeks. So initially there was not a significant difference but gradually the gap between people in the two conditions grew. After about 18 sessions I should say. So that's one study finding that there is an advantage to having a specific therapeutic technique at least after a certain number of sessions. Okay, so, but given that, when you compare the specific therapeutic techniques, there's not much of a difference. There's a growing body of evidence into what are the variables that the different therapeutic techniques have in common that explain why therapy succeeds. Additionally, there is research into what are the variables, not in the therapist, but in the client, that predict therapeutic success. If there's not much of a difference between CBT and psychodynamic and so on, what are some other things that might be important? I'm not going to go into great detail, but just to list some of the book mentions. There's evidence that openness is important, not in the sense of the big five trait, but here it's defined as a willingness to invest yourself in the therapy process. Some people think that therapy is like a pill, you just show up and clock in your hour and you'll get better, but you have to be willing to go through the work. It's not just a matter of showing up, you do have to be willing to put in the work on your part. Another variable is self-relatedness, which is an ability to experience and understand your own emotions. This may not be necessary, but it is a variable that predicts increased success and capacity to benefit from therapy. Another thing that people are looking at is what's called a dose dependent, or I'm sorry, a dose response effect, which is just, not just is the therapeutic technique effective or not, but how much bang do you get for your buck, right? How many sessions does it take to yield clinically significant benefits? So, one criticism that I mentioned of psychoanalysis is it may take too long, right? If you're not loaded down heavy, it might not be in your interest to, you know, spend the rest of your life seeing an analyst. I can't quote chapter and verse here, but some have argued that... BT is better on that front, for example, that it's more efficient. You get more benefit per session. And then as far as variables... that the therapy technique has that are important, these are called common factors. So these are variables that different therapeutic techniques can have in common that explain why the therapy works. So, even though the specific technique might not matter, it seems to matter that these be there at least to some degree. So the book lists faith in the therapist, having some confidence that this will yield some benefit. Some kind of plausible explanation for their problems. So, early on I drew a distinction between insight-oriented therapies and symptom-oriented therapies. That distinction is a little bit arbitrary. This indicates that it's important that there be some degree of insight, some degree of explaining, you know, this is why you have the problems that you do. Relatedly, it's important to give people an alternative way of looking at themselves and their problems, some kind of new way of viewing their situation. That's of course something that the cognitive people emphasize, but that has been integrated into other techniques as well. One that the humanists emphasize, and this again is no longer unique to humanistic therapy, other techniques have, practitioners and other techniques have integrated this as well, is a protective setting in which clients can experience and express their feelings. So that's considered to be important. An opportunity to practice new behaviors, and increase optimism and self-efficacy. So, not to go into too much detail, but those are some of the common factors that the book mentions. One term that's not in the book that I won't test you on, but nowadays, most psychotherapists are to some degree eclectic. Eclectic means you pick and choose. You integrate variables from different techniques. So you're not exclusively cognitive or exclusively psychoanalytic. You're willing to draw on the insights of different techniques. If you Google counselors in Edmonton and look at their theoretical orientations, most of them will list more than one. So nowadays most of them are eclectic. The book mentions one study on a specific kind of therapy called behavioral activation as one of those asides. I'm not going to go into detail there. I've tried to restrict myself in this chapter to meta-analyses because any one study can have problems, and actually in this specific case, for whatever it's worth, right within the book it says, so it compares cognitive therapy to this kind of unusual therapy called behavioral activation, and to drug therapy. One thing it mentions in passing, the attrition rate is very different for the different conditions. You don't need to know this for the test, but attrition is how many people leave. ...the experiment, which happens sometimes. And in the drug condition, the attrition rate was 44%, whereas in the other two conditions it was under 20%. That makes it very hard to interpret the results, because now you don't know if the differences between the groups are the result of the intervention, or if they're because... The people who left are different from the people who stayed. This is a good thing to keep your eye out for when you're looking at studies. Again, I won't test you on that, but just a little thing to be aware of. Okay, the next section... is on biological approaches to treatment. The most common one, and the one the book spends the most time talking about, is drug therapies. Sometimes called psychopharmacology. These are often used as the first line of defense against various psychological disorders. As I'm going to kind of say throughout, I think that's a little bit unfortunate. The reason it's done that way is, look, it's just simpler. It's easier for the government to give money to just give people pills. You just buy the pill and that's it. One thing I'll mention for some of the types of drugs, it's often the case that therapy is as effective or more effective with the value-added bonus of no side effects. Any medication you take will have the possibility of side effects. So hopefully in the future, therapy is more of a first-line intervention. But nowadays, unfortunately, in my view, it tends to be drug therapies. The first family of psychiatric medication that you need to know is anti-anxiety drugs. Probably the most studied are benzos, I'll just call for short, benzodiazepines, which includes Xanax and Valium and various others. And these all work on the GABA system. GABA is an inhibitory neurotransmitter. So, inhibitory meaning when they are sent from one neuron to another, they decrease the chance that the next neuron will send a signal. Alcohol acts on the GABA system as well. So it kind of slows you down. So they increase GABA transmission, which makes sense, right? So if you're constantly anxious, these will have a calming effect, kind of slow you down and relax you. Unlike some of the other ones we will look at, these are extremely addictive. I actually know people personally who were prescribed these. Getting off them was extremely difficult. You have to like micro-taper off of them. So there's a growing consensus that these should only be used for short-term intervention. They are effective at calming people down if someone is having a kind of mental health emergency and they just need to be calmed down. help to sleep and relax. These can be effective. But prescribing them as a long-term treatment, yeah, let's put it this way, I would strongly advise against that based on people I know who have done that. So those are anti-anxiety drugs. So you should know that the names, those are probably the two most common. Both of them fall under the umbrella of benzodiazepines. Any questions on the anti-anxiety drugs? Next. Most of these, almost all of the drugs that fall under the umbrella of antidepressants, act on the serotonin system. Some of them act on other neurotransmitter systems as well. So, the first example is MAO inhibitors, monoamine oxidase inhibitors. Monoamine oxidase... So let's say this is the tip of an axon, and this is a dendrite. So this is the neuron that's sending neurotransmitters to the dendrite, which is what receives neurotransmitters. So there's neurotransmitters in here, and then when a charge comes to here, they get sent to the dendrite. Monoamine oxidase breaks down some of these, just dissolves them and recycles them. Monoamine oxidase inhibitors stop that. Hey, come on man, don't break them down, give them a chance. Which means there's more serotonin and other neurotransmitters that are freed up to be sent across. So it's stopping something from breaking down the neurotransmitters. As I say, those act on serotonin and multiple other types. I think norepinephrine and dopamine, if my memory is correct. So that's those. But by far, nowadays, the most commonly... Prescribed antidepressants are SSRIs. These are used actually for a number of different conditions. So these are similar in that they kind of do a double negative. So this stands for selective, meaning only, serotonin reuptake inhibitors. So these only act on the serotonin system. The way they work is, so serotonin gets sent across the sinus, and some of them don't bind to the dendrite in time. None of the dendrite receptors swipe right on the serotonin. And what the axon will do is it will take, so let's say these all go across. It will take these back. It will say, okay, you failed. You did not get across in time. So reuptake occurs. They take back some of the serotonin and recycle it. SSRIs stop that from happening. You know, come on, give them a chance. And therefore, it increases how much serotonin gets sent across the cypress. So by preventing reuptake, more serotonin gets transmitted. So that's how they work. Now, I think some people have the impression that these, that antidepressants will make you happy, they're like a happy drug, but that is not how they work. One way we know, I'll just say that... When you take them, it has this effect almost immediately. It will increase serotonin transmission very quickly, but they don't have a measurable effect on depression for several weeks. So whatever effect they're having, it's not directly via increasing serotonin transmission. It's probably some downstream effect. There's still evidence that it leads to hippocampal growth, growth in the hippocampus, which can be associated with benefits, but it's not like a quick, happy drug. Now, how effective are antidepressants? These are the most commonly prescribed psychiatric drugs nowadays. Probably many of you are on them, or a non-trivial number of you are on them. And I want to say a bit about their efficacy. So again, I'll restrict myself to large meta-analyses. There was a meta-analysis that looked at lots of randomized controlled trials, so studies where you get a group, you randomly assign them to two groups, you give one of them the SSRI and one group the placebo. So they combined lots of these studies, over 27,000 people, If you use the Hamilton Depression Rating Scale, there's a few different measures. I mentioned the Beck Depression Inventory last time. Another commonly used one is the HAMD, the Hamilton Depression Rating Scale. You don't need to know the details, but just for a bit of context, the scale is out of 52, and 24 and up is considered severe depression. So it's got quite a wide range. There is a statistically significant difference. Between the SSRI groups and the placebo groups, how much? About two points on the HAMD. So both groups will go down. If you take a placebo, you will feel better. The SSRI groups go down about two points more on the HAMD than the placebo group. So on a scale of up to 52, that's not a very big effect. And there's another meta-analysis that found that this effect is only statistically significant for severe depression. For people who have mild to moderate depression, there is no detectable difference between the SSRI and the placebo. So my own view, now I'm not a clinician, so take everything I say with a grain of salt, is that you should only take SSRIs if you are severely depressed. If someone's at risk of killing themselves, you should do whatever you can to stay alive, or to keep the person alive. So that makes sense to me, but my view is that it is overprescribed. It's often used as the first response to someone who's depressed, and given the evidence, I think that's probably not. ...a good idea, especially given the fact that, like I said, every drug has risks of side effects. And SSRIs are no exception. There's growing evidence of sexual side effects. Serotonin is an important part of the sexual response system. So given how small the benefit is, I think it should be taken more cautiously. And one small rant I want to go on. I don't know if any of you have seen this on the train. How many of you have seen this on LRT? Just okay is not okay. This is an ad for an antidepressant. I just want to say I strongly disagree with this. Life is suffering. Just okay is okay. If you're doing okay, you should be on your knees every night thanking God that you're doing okay. To use this as a... because most people are just okay. Like, that's kind of the most you can hope for. So, I just want to say, as a soon-to-be PhD in psychology, I very strongly disagree with this. Okay, and one other thing. One other thing that people should be aware of, and there's lots of data here. Taking antidepressants increases your risk of relapse when you go off the road. Yes sir, in the back. Do you think those ads should be legal? Sorry? Do you think the ads should be legal? Oh, yeah. Antidepressants. Yeah, this isn't a political or an FX class. I won't say my... The question was, should antidepressants ads be illegal? That specific one should be. I'll go that far. I haven't thought enough about whether they should be illegal in general. That's an interesting question. There was a lawsuit against Facebook about this. Oh, I don't know. I don't follow it that closely. Maybe I should read more and then teach a class on medical ethics, but I won't go that far. I'm not sure if I think this should be illegal. But, in any case, this is something I'll quickly point to. These are the different types of antidepressants, and they are ranked by how many... neurotransmitters they act on. So the MAO inhibitors that we talked about act on several neurotransmitters, whereas the SSRIs only act on one. And this is the rate of relapse after you stop using them. And PBO is placebo. And this makes sense because whenever you go on a medication, you can build up tolerance for it, such that when you go off of them, there's kind of a reaction your body has because it's dependent on taking them. This is another thing I think to human life. And as I mentioned in passing at the beginning of this section, These medications are roughly as effective as different types of therapy such as CBT. That meta-analysis I mentioned last class that compared the different types of therapy for depression, they also include included people who were on antidepressants. And what you find is, again, as is often the case, roughly equally effective. At least in the short term. In the long term, actually, CBT has an edge over antidepressants. Which makes sense, right? Because you're building skills that enable you to deal with it. And as I said, there's the value-added bonus that CBT does not give you side effects. So, now it does cost more money, but that's something important to keep in mind. The last thing I have to say about antidepressants, there was a recent excellent study on something called the chemical imbalance theory. So for a long time, these medications, including actually anti-anxiety drugs, were marked as a chemical imbalance. marketed by clinicians saying that these are reversing an underlying chemical imbalance. So there are these studies that I mentioned that find that these drugs are measurably better than placebo for reducing depressive symptoms, especially for severe depression, and they increase serotonin transmission. So what people argue is, well, that shows that low serotonin was what caused the depression. As I mentioned in a previous class, that's not a very good argument, because the mere fact that changing your brain chemistry makes you happier doesn't mean that the initial sadness was caused by a brain chemistry problem. I think I jokingly said, you know, if I... give you heroin, you'll be happier, at least for a while. That does not show that low heroin was the initial problem. And as I said, there was a recent meta-analysis that looked at all of the studies that actually measure the level of heroin in the body. level of serotonin in depressed people. That's a better way to do it. Now, you can't measure brain serotonin directly, but there are various proxies that you can use. And when you combine all the data, there is no good evidence that depressed people have lower levels of serotonin or some kind of abnormal serotonin system. So this was work done by Joanna Bonkrieff, who's a psychiatrist in the UK. So I'll show a video of her discussing this meta-analysis that she did. Okay, so they go on for a while. Obviously we're not going to watch the whole video, but that was a very widely cited meta-analysis. And I would say now most people don't argue that in a straightforward way, depression is caused by low serotonin. Now, I want to be clear. I'm not saying that we should never use these drugs. They have no use. As I've now said a few times, look, if someone is severely depressed or at risk of suicide, do whatever you can to keep the person alive, obviously. But like any medical intervention, they will have some risk. It's so important to keep that in mind. The only other thing I have to say about the mood section is there's another drug that's used specifically for bipolar, which is lithium carbonate, or science has called lithium. So it's literally like a lithium substance. This seems to have a stabilizing effect on mood. So bipolar, remember, has extremes like mania and depression. Lithium helps to keep you stable. Any questions on antidepressants before you move on to antipsychotics? Yes? The MAO dilutes the neurotransmitters in the axon diluter, right? Not dilutes. It's going to make it so there's more of that. So inhibitor, MAO itself. Oh, yes, good. So yes, MAO, yes, dilutes how many neurotransmitters, like it eats some of them or whatever, like dissolves them. The MAO inhibitors stop that. So, yes. Any other questions? Okay, the next category of drugs is antipsychotics. So psychosis, or psychotic conditions, is an umbrella that includes any conditions with hallucinations. delusions, other kinds of irrational propensities. So the type of psychosis we spent the most time talking about is schizophrenia. That's the only one you really need to know. There are other more mild types of psychosis, but the type that's been most widely studied is schizophrenia. So you'll recall that there are some people who have argued that Too much dopamine transmission is involved in schizophrenia. I don't know as much about that as I do about the serotonin theory of depression, but my impression is the evidence is stronger there for a connection between dopamine problems and schizophrenia. So as you can probably guess, antipsychotics reduce dopamine transmission. at least the main kinds. Now one downside of this is it can produce a condition called tardive dyskinesia. This is a motor problem. So dopamine is involved in a number of different But one thing it's involved in is initiating voluntary movement. And so, if you mess with the dopamine system, you can get this condition. This is somewhat similar to Parkinson's disease, which is also a motor condition. There's a kind of interesting relationship between schizophrenia and Parkinson's in that they're sort of opposites. So schizophrenia, there's some evidence that high dopamine is involved. Parkinson's, we know for sure, has to do with low dopamine. They're dopaminergic. regions of the brain that are damaged in Parkinson's or that deteriorate in Parkinson's. And so the treatment for Parkinson's is L-DOPA. You don't need to know that for the test, but it increases dopamine transmission. And it produces symptoms kind of like schizophrenia. That's kind of a side effect, is you go a little kooky. You can have some schizophrenia-like symptoms. And then for schizophrenia, the treatment is to reduce dopamine transmission. And then you get this, which is kind of like Parkinson's. You don't need to know about the Parkinson's case. That's just to reinforce the point that there does seem to be this relationship between... high dopamine and schizophrenia-like symptoms, and low dopamine and Parkinson's-like symptoms. So this is the name for a Parkinson's-like set of symptoms that results from taking antipsychotics. Any questions about that? I have less to say about the antipsychotics, but any questions about that? conditions like schizophrenia. When you're on drug therapy, do you just like get prescribed for this new life or is it like... That's a good question. So some people do need to be on them for life. I know it's the case that the antipsychotics target the positive symptoms more, so like the hallucinations, the delusions, and that those tend to be worse in your 20s and 30s. So maybe it's okay to go off them later in life if those aren't as severe. Don't quote me on that, though. I'm not a clinician, but that's my recollection of that. Now as I say, these antipsychotics, the ones that target dopamine, are more effective for positive symptoms. You do not need to know this for the test, but there are a growing set of what are called atypical antipsychotics that work in other ways, and they tend to be more effective for the negative symptoms, like flat affect and things like that. Another thing I'll mention that's not listed in the key terms, so don't worry about it, but there's also another category of drug that's used a lot for conditions, which is stimulants. Different types of stimulants, which increase brain activity, which speed the brain up. This is commonly used for ADHD. which I always thought was kind of strange, because ADHD is like having too much energy and being too inattentive, but there is evidence that they produce some benefit. One conjecture could be that everything is kind of boring to them. They find nothing stimulating, so you give them some stimulants, and now they're able to pay attention, because they're able to find it more exciting. That's a little bit conjectural, but there's some evidence that stimulants are effective for reducing ADHD symptoms. Though a very strong argument to be made that maybe they are also over-prescribed. Okay, that's the end of the section on drugs. The next type of intervention is a little savage. I feel like we'll look back on this and be a little bit surprised that we ever did this. But it does produce benefits. I'm referring here to electroconvulsive therapy, or ECT. So, this is today most commonly used for treatment-resistant depression. It used to be used more broadly, but that is one issue for which the evidence is quite strong that this can be beneficial. So by treatment-resistant, I mean you gave them an antidepressant, maybe you tried a different antidepressant, you tried some therapy, and the person is still suicidally depressed, so at serious risk of taking their own life. Obviously with the consent of the patient, what you do is you lie them down, you give them an anesthetic so you put them to sleep, you tie their limbs down so they don't hurt themselves. Although actually in the video I forget if they do. I have a video of this. And then you run an electric... ...current through their brain to induce a brief seizure. And believe it or not, this is actually quite effective at reducing serious depressive symptoms. The main risk is temporary amnesia. The person will sometimes have memory problems after. They are usually temporary, but that's the main risk. But again, if someone is at serious risk of killing themselves, sometimes you will do whatever is available. Now, if you're squeamish, you can close your eyes and leave for a few minutes, but I actually have a video of this in action, so this is what ECT looks like. Okay, I'll stop there. Okay, so that's ECT. Another intervention that's even more rare is psychosurgery. So this involves actual, you know, either cutting of different parts or even removal of small parts. One that used to be used a lot was the prefrontal lobotomy. This was used on very difficult... or even violent mental patients. It involved, and sorry it's kind of graphic, but sticking ice pick-like instruments beside the eyes and severing connections in the right parts of the frontal cortex, which often made patients more malleable and compliant. Believe it or not, this was done to JFK's sister. She was a very serious, had very serious issues. Nowadays, we never do that. Yes? Oh, I didn't know that. Okay, this person says Queen Elizabeth's sister. I don't know, but that wouldn't surprise me. So it was fairly widespread. The book lists a few more minor examples that are still done today. You don't need to know the details, but in very extreme cases, this is sometimes used. The book has a discussion of deinstitutionalization. This occurred in the 50s and 60s. There used to be significantly more long-term psychiatric hospitals where people would stay essentially for life. if they were too difficult to deal with or had too much trouble integrating into society. Many of them had severe schizophrenia. Following the development of psychiatric drugs like antipsychotics, it was thought that... that maybe these people should be released and could be given long-term outpatient care. This was, I think it's fair to say, a profound failure. This led to a significant increase in homelessness. It turns out the medication was, in many cases, not sufficient to reintegrate them into society. I'm not saying the institutions were good. They were obviously problematic. It's understandable why they were shut down. But there was not sufficient effort to successfully... reintegrating them, so many of these people wound up becoming homeless. And then the last pair of terms have to do with prevention. So there's a growing move towards prevention. It's often a more cost-effective way of dealing with, or I guess not dealing with conditions, but stopping them before they arise. And the two types the book mentions are situation-focused prevention and competency-focused prevention. Situation-focused prevention targets the environmental causes of psychiatric disorders, so poverty, crime, or child abuse, or things like lead in the water. That's one that's been widely studied. So getting rid of things like that is a way of preventing disorders from emerging. And competency-focused prevention is about teaching people coping mechanisms and resilience before they develop a disorder. It's often good to target that towards people who are at risk. So that's the other kind of prevention. Okay, and that is the last term in this course. Any questions? Okay, so I know some of you have been with me for two minutes. ...courses now, and I thought, do I have any, like, final words for this course, or for this pair of courses for some of you? And one thing I'm in the mood to say after going through Chapter 17 is I would strongly encourage you to treat this book and psychology in general as a work in progress, right? This is why I encourage you all to not engage in self-diagnosis. psychology is a human activity and is therefore very fallible like anything is so this is not the final work this is a work in progress maybe some of you will contribute to furthering it along but don't take any of it as infallible That's one thing you discover as you get older, is that everything human is very fallible. I have found that the closer I've gotten to the scientific process, in a way the more skeptical I've become of it. I think it's the best we have. I think science is the most reliable way of acquiring knowledge that we have, but it is still very much a human activity. My mom had the same reaction. She was, uh, she got on the city council. She always loved politics. And the closer she got to it, the more she was like, wow, this is, like, very human. The people who don't study in high school grow up to run the world. Those people get jobs when they grow up, so. And, uh, the same is true of science. Okay, so... I'm mindful of the time. I actually don't think we'll have time to do the game unless we really rushed. Hopefully none of you are too devastated by this. Any questions about anything in the course? The rest of the time is... is for you all, so any questions, because the final on Thursday is Q&A. Can you go over bipolar 1 and 2 and type 1 and 2 specifically? Yes, so bipolar 1 and 2, so bipolar 1 is mania, so both 1 and 2 have depression, and that's the same, but bipolar 1 has full-blown mania, bipolar 2 only has hypo mania, so kind of like dying mania. Not quite full-blown. for type 1 and 2 schizophrenia type 1 is more positive symptoms delusions, hallucinations things like that type 2 is more of the negative symptoms like flat effect Additionally, Type 1 is often more sudden. There are more people in the Type 1 umbrella who are perfectly normal, well-adjusted people, and then in their late teens or early 20s, they just lose their mind. Type 2 often emerges more gradually, and unfortunately is therefore associated with less likelihood of successful, a lower likelihood of successful treatment. Any other questions? Yes. Say again? Oh, prevalence. You do not need to know the prevalence rates for different disorders. Kind of interesting information, but you do not need to memorize those. Yes. You definitely need to know the symptoms of disorders. Those are good to know. Yes. Yeah, I would say all of that is fair game. So anything on the key terms, as usual, from chapters 2, 9, and 12 through 15, all of that is fair game. So just a reminder. The final on Thursday is 70 multiple choice. 30 of them come from those first chapters. Anything is fair game. And then 40 will come from chapter 16 and 17, 20 each. No written, there's no written on the final. Now I will say, having said that, if you're going to be efficient, I would recommend focusing more on the big ideas from the early chapters. It's not to say that the details can't come up, but there's a better chance of the big ideas coming up. I think someone over here had their hand up first. I was in the same place. Same place. Yep. Moving back to developmental... Yeah, all that's fair game. Yeah. Any other questions? Anything in the book is fair game. Questions? Yeah? What's the difference between exposure and response? So technically, so the question was what's the difference between exposure response prevention and systematic desensitization? Technically, systematic desensitization falls under the umbrella of exposure response prevention. Reaction response prevention just means you expose them to something that induces anxiety normally and prevent them from doing what they normally do. In the case of OCD, that means preventing the compulsive ritualistic behavior. In the case of a phobia, it means preventing the avoidance, preventing them from running away from it like they usually do. Systematic desensitization just means doing that slowly, step by step, starting at the bottom of the anxiety hierarchy and working your way up. Can you go over the biomarkers for dementia or Alzheimer's? Yeah, Alzheimer's, there's just two. So there's two biomarkers for Alzheimer's, amyloid plaques and neurofibrillary tangles. You don't need to know what they look like. Those are just two things you can see on the neurons of people with Alzheimer's. They're one of the things that distinguishes Alzheimer's from just ordinary dementia. I just want to know if this definition is correct, but like this all therapy, like... Is the definition like it brings and just talks to immediate awareness so that like can be whole again? Not quite, it's thought therapy. The word I would use is integration. You're trying to integrate your experiences into a whole. So people may feel scattered or disconnected in their memories or experiences. Gestalt therapy, the goal of gestalt therapy is to bring them into a whole, to integrate them. Just like in perception, the gestalt psychologists study the ways in which we organize things into patterns or wholes. The therapist thought we should do something similar with our experiences and our methods. I'm sorry, was the final exam weighted towards chapter 16 and 17 or 16 and 17? Yes, it is. So just as a shared number. So it's 70 questions, 20 of them from 16 and 20 from 17, and then 30 from all the others. other. So it works out to, I think, like four or five per chapter. The reason for that, as I think I've mentioned, is for the other chapters, you're getting tested on them twice, in the final and in the other tests. So it works out to like seven or eight percent per chapter, as far as the multiple choice goes. Yes, it's here on Thursday during normal class time. There's nothing during finals week. As of Thursday, you are all done. That's the end. Yep. Yep, like everything I said today would be fair game. So yeah, like the names of the drugs, how they work, that's all fair game too. No? For the personality disorders, I went through all of them mostly as a point of interest. The only two I would worry about are antisocial and bullying. Okay, so some people are leaving. We'll call it there. If you have more questions, come and talk to me. I will see you all on Thursday. And if I don't see you after this course, good luck with your education.

Alright guys, let's get started. Okay, wrap up your conversations. It's the last lecture before the final.

So, we'll wrap up chapter 17, we'll do our little review game, and then we'll leave the remaining time for any questions that you have about any of the content in the course. How many of you got a chance to see the eclipse, by the way, yesterday? Not very many. Even from here, it's still pretty cool.

Okay, one thing I forgot to mention last class. So we were talking about the efficacy of the different types of therapy, and how there are big meta-analyses indicating that there's probably not that big of a difference between the different types. But I forgot to mention there was another meta-analysis that compared specifically CBT, which is probably the most commonly used, it's a cognitive behavioral therapy, it compared that with generic counseling. Which is closer to a good placebo, right?

Just general counseling without any specific therapeutic strategy. And that meta-analysis had over 30,000 people and it was found that there was an advantage for CBT. They defined recovery as your depression score declining by a certain number of points.

And when you... use that definition, 60% of people who were undergoing CBT recovered, whereas only 40% in the generic counseling conditions recovered. Now, this advantage only became...

significant after about 18 weeks. So initially there was not a significant difference but gradually the gap between people in the two conditions grew. After about 18 sessions I should say.

So that's one study finding that there is an advantage to having a specific therapeutic technique at least after a certain number of sessions. Okay, so, but given that, when you compare the specific therapeutic techniques, there's not much of a difference. There's a growing body of evidence into what are the variables that the different therapeutic techniques have in common that explain why therapy succeeds.

Additionally, there is research into what are the variables, not in the therapist, but in the client, that predict therapeutic success. If there's not much of a difference between CBT and psychodynamic and so on, what are some other things that might be important? I'm not going to go into great detail, but just to list some of the book mentions.

There's evidence that openness is important, not in the sense of the big five trait, but here it's defined as a willingness to invest yourself in the therapy process. Some people think that therapy is like a pill, you just show up and clock in your hour and you'll get better, but you have to be willing to go through the work. It's not just a matter of showing up, you do have to be willing to put in the work on your part.

Another variable is self-relatedness, which is an ability to experience and understand your own emotions. This may not be necessary, but it is a variable that predicts increased success and capacity to benefit from therapy. Another thing that people are looking at is what's called a dose dependent, or I'm sorry, a dose response effect, which is just, not just is the therapeutic technique effective or not, but how much bang do you get for your buck, right? How many sessions does it take to yield clinically significant benefits? So, one criticism that I mentioned of psychoanalysis is it may take too long, right?

If you're not loaded down heavy, it might not be in your interest to, you know, spend the rest of your life seeing an analyst. I can't quote chapter and verse here, but some have argued that... BT is better on that front, for example, that it's more efficient.

You get more benefit per session. And then as far as variables... that the therapy technique has that are important, these are called common factors.

So these are variables that different therapeutic techniques can have in common that explain why the therapy works. So, even though the specific technique might not matter, it seems to matter that these be there at least to some degree. So the book lists faith in the therapist, having some confidence that this will yield some benefit. Some kind of plausible explanation for their problems. So, early on I drew a distinction between insight-oriented therapies and symptom-oriented therapies.

That distinction is a little bit arbitrary. This indicates that it's important that there be some degree of insight, some degree of explaining, you know, this is why you have the problems that you do. Relatedly, it's important to give people an alternative way of looking at themselves and their problems, some kind of new way of viewing their situation. That's of course something that the cognitive people emphasize, but that has been integrated into other techniques as well.

One that the humanists emphasize, and this again is no longer unique to humanistic therapy, other techniques have, practitioners and other techniques have integrated this as well, is a protective setting in which clients can experience and express their feelings. So that's considered to be important. An opportunity to practice new behaviors, and increase optimism and self-efficacy. So, not to go into too much detail, but those are some of the common factors that the book mentions.

One term that's not in the book that I won't test you on, but nowadays, most psychotherapists are to some degree eclectic. Eclectic means you pick and choose. You integrate variables from different techniques.

So you're not exclusively cognitive or exclusively psychoanalytic. You're willing to draw on the insights of different techniques. If you Google counselors in Edmonton and look at their theoretical orientations, most of them will list more than one.

So nowadays most of them are eclectic. The book mentions one study on a specific kind of therapy called behavioral activation as one of those asides. I'm not going to go into detail there.

I've tried to restrict myself in this chapter to meta-analyses because any one study can have problems, and actually in this specific case, for whatever it's worth, right within the book it says, so it compares cognitive therapy to this kind of unusual therapy called behavioral activation, and to drug therapy. One thing it mentions in passing, the attrition rate is very different for the different conditions. You don't need to know this for the test, but attrition is how many people leave.

...the experiment, which happens sometimes. And in the drug condition, the attrition rate was 44%, whereas in the other two conditions it was under 20%. That makes it very hard to interpret the results, because now you don't know if the differences between the groups are the result of the intervention, or if they're because... The people who left are different from the people who stayed.

This is a good thing to keep your eye out for when you're looking at studies. Again, I won't test you on that, but just a little thing to be aware of. Okay, the next section... is on biological approaches to treatment.

The most common one, and the one the book spends the most time talking about, is drug therapies. Sometimes called psychopharmacology. These are often used as the first line of defense against various psychological disorders. As I'm going to kind of say throughout, I think that's a little bit unfortunate. The reason it's done that way is, look, it's just simpler.

It's easier for the government to give money to just give people pills. You just buy the pill and that's it. One thing I'll mention for some of the types of drugs, it's often the case that therapy is as effective or more effective with the value-added bonus of no side effects.

Any medication you take will have the possibility of side effects. So hopefully in the future, therapy is more of a first-line intervention. But nowadays, unfortunately, in my view, it tends to be drug therapies.

The first family of psychiatric medication that you need to know is anti-anxiety drugs. Probably the most studied are benzos, I'll just call for short, benzodiazepines, which includes Xanax and Valium and various others. And these all work on the GABA system.

GABA is an inhibitory neurotransmitter. So, inhibitory meaning when they are sent from one neuron to another, they decrease the chance that the next neuron will send a signal. Alcohol acts on the GABA system as well.

So it kind of slows you down. So they increase GABA transmission, which makes sense, right? So if you're constantly anxious, these will have a calming effect, kind of slow you down and relax you. Unlike some of the other ones we will look at, these are extremely addictive. I actually know people personally who were prescribed these.

Getting off them was extremely difficult. You have to like micro-taper off of them. So there's a growing consensus that these should only be used for short-term intervention.

They are effective at calming people down if someone is having a kind of mental health emergency and they just need to be calmed down. help to sleep and relax. These can be effective.

But prescribing them as a long-term treatment, yeah, let's put it this way, I would strongly advise against that based on people I know who have done that. So those are anti-anxiety drugs. So you should know that the names, those are probably the two most common.

Both of them fall under the umbrella of benzodiazepines. Any questions on the anti-anxiety drugs? Next. Most of these, almost all of the drugs that fall under the umbrella of antidepressants, act on the serotonin system. Some of them act on other neurotransmitter systems as well.

So, the first example is MAO inhibitors, monoamine oxidase inhibitors. Monoamine oxidase... So let's say this is the tip of an axon, and this is a dendrite. So this is the neuron that's sending neurotransmitters to the dendrite, which is what receives neurotransmitters.

So there's neurotransmitters in here, and then when a charge comes to here, they get sent to the dendrite. Monoamine oxidase breaks down some of these, just dissolves them and recycles them. Monoamine oxidase inhibitors stop that. Hey, come on man, don't break them down, give them a chance. Which means there's more serotonin and other neurotransmitters that are freed up to be sent across.

So it's stopping something from breaking down the neurotransmitters. As I say, those act on serotonin and multiple other types. I think norepinephrine and dopamine, if my memory is correct. So that's those.

But by far, nowadays, the most commonly... Prescribed antidepressants are SSRIs. These are used actually for a number of different conditions.

So these are similar in that they kind of do a double negative. So this stands for selective, meaning only, serotonin reuptake inhibitors. So these only act on the serotonin system. The way they work is, so serotonin gets sent across the sinus, and some of them don't bind to the dendrite in time. None of the dendrite receptors swipe right on the serotonin.

And what the axon will do is it will take, so let's say these all go across. It will take these back. It will say, okay, you failed.

You did not get across in time. So reuptake occurs. They take back some of the serotonin and recycle it.

SSRIs stop that from happening. You know, come on, give them a chance. And therefore, it increases how much serotonin gets sent across the cypress. So by preventing reuptake, more serotonin gets transmitted. So that's how they work.

Now, I think some people have the impression that these, that antidepressants will make you happy, they're like a happy drug, but that is not how they work. One way we know, I'll just say that... When you take them, it has this effect almost immediately. It will increase serotonin transmission very quickly, but they don't have a measurable effect on depression for several weeks. So whatever effect they're having, it's not directly via increasing serotonin transmission.

It's probably some downstream effect. There's still evidence that it leads to hippocampal growth, growth in the hippocampus, which can be associated with benefits, but it's not like a quick, happy drug. Now, how effective are antidepressants? These are the most commonly prescribed psychiatric drugs nowadays.

Probably many of you are on them, or a non-trivial number of you are on them. And I want to say a bit about their efficacy. So again, I'll restrict myself to large meta-analyses. There was a meta-analysis that looked at lots of randomized controlled trials, so studies where you get a group, you randomly assign them to two groups, you give one of them the SSRI and one group the placebo. So they combined lots of these studies, over 27,000 people, If you use the Hamilton Depression Rating Scale, there's a few different measures.

I mentioned the Beck Depression Inventory last time. Another commonly used one is the HAMD, the Hamilton Depression Rating Scale. You don't need to know the details, but just for a bit of context, the scale is out of 52, and 24 and up is considered severe depression. So it's got quite a wide range. There is a statistically significant difference.

Between the SSRI groups and the placebo groups, how much? About two points on the HAMD. So both groups will go down. If you take a placebo, you will feel better. The SSRI groups go down about two points more on the HAMD than the placebo group.

So on a scale of up to 52, that's not a very big effect. And there's another meta-analysis that found that this effect is only statistically significant for severe depression. For people who have mild to moderate depression, there is no detectable difference between the SSRI and the placebo.

So my own view, now I'm not a clinician, so take everything I say with a grain of salt, is that you should only take SSRIs if you are severely depressed. If someone's at risk of killing themselves, you should do whatever you can to stay alive, or to keep the person alive. So that makes sense to me, but my view is that it is overprescribed.

It's often used as the first response to someone who's depressed, and given the evidence, I think that's probably not. ...a good idea, especially given the fact that, like I said, every drug has risks of side effects. And SSRIs are no exception. There's growing evidence of sexual side effects.

Serotonin is an important part of the sexual response system. So given how small the benefit is, I think it should be taken more cautiously. And one small rant I want to go on. I don't know if any of you have seen this on the train.

How many of you have seen this on LRT? Just okay is not okay. This is an ad for an antidepressant.

I just want to say I strongly disagree with this. Life is suffering. Just okay is okay. If you're doing okay, you should be on your knees every night thanking God that you're doing okay. To use this as a...

because most people are just okay. Like, that's kind of the most you can hope for. So, I just want to say, as a soon-to-be PhD in psychology, I very strongly disagree with this. Okay, and one other thing. One other thing that people should be aware of, and there's lots of data here.

Taking antidepressants increases your risk of relapse when you go off the road. Yes sir, in the back. Do you think those ads should be legal?

Sorry? Do you think the ads should be legal? Oh, yeah. Antidepressants. Yeah, this isn't a political or an FX class.

I won't say my... The question was, should antidepressants ads be illegal? That specific one should be.

I'll go that far. I haven't thought enough about whether they should be illegal in general. That's an interesting question. There was a lawsuit against Facebook about this.

Oh, I don't know. I don't follow it that closely. Maybe I should read more and then teach a class on medical ethics, but I won't go that far.

I'm not sure if I think this should be illegal. But, in any case, this is something I'll quickly point to. These are the different types of antidepressants, and they are ranked by how many... neurotransmitters they act on. So the MAO inhibitors that we talked about act on several neurotransmitters, whereas the SSRIs only act on one.

And this is the rate of relapse after you stop using them. And PBO is placebo. And this makes sense because whenever you go on a medication, you can build up tolerance for it, such that when you go off of them, there's kind of a reaction your body has because it's dependent on taking them. This is another thing I think to human life. And as I mentioned in passing at the beginning of this section, These medications are roughly as effective as different types of therapy such as CBT.

That meta-analysis I mentioned last class that compared the different types of therapy for depression, they also include included people who were on antidepressants. And what you find is, again, as is often the case, roughly equally effective. At least in the short term. In the long term, actually, CBT has an edge over antidepressants. Which makes sense, right?

Because you're building skills that enable you to deal with it. And as I said, there's the value-added bonus that CBT does not give you side effects. So, now it does cost more money, but that's something important to keep in mind.

The last thing I have to say about antidepressants, there was a recent excellent study on something called the chemical imbalance theory. So for a long time, these medications, including actually anti-anxiety drugs, were marked as a chemical imbalance. marketed by clinicians saying that these are reversing an underlying chemical imbalance.

So there are these studies that I mentioned that find that these drugs are measurably better than placebo for reducing depressive symptoms, especially for severe depression, and they increase serotonin transmission. So what people argue is, well, that shows that low serotonin was what caused the depression. As I mentioned in a previous class, that's not a very good argument, because the mere fact that changing your brain chemistry makes you happier doesn't mean that the initial sadness was caused by a brain chemistry problem.

I think I jokingly said, you know, if I... give you heroin, you'll be happier, at least for a while. That does not show that low heroin was the initial problem.

And as I said, there was a recent meta-analysis that looked at all of the studies that actually measure the level of heroin in the body. level of serotonin in depressed people. That's a better way to do it.

Now, you can't measure brain serotonin directly, but there are various proxies that you can use. And when you combine all the data, there is no good evidence that depressed people have lower levels of serotonin or some kind of abnormal serotonin system. So this was work done by Joanna Bonkrieff, who's a psychiatrist in the UK. So I'll show a video of her discussing this meta-analysis that she did. Okay, so they go on for a while.

Obviously we're not going to watch the whole video, but that was a very widely cited meta-analysis. And I would say now most people don't argue that in a straightforward way, depression is caused by low serotonin. Now, I want to be clear.

I'm not saying that we should never use these drugs. They have no use. As I've now said a few times, look, if someone is severely depressed or at risk of suicide, do whatever you can to keep the person alive, obviously. But like any medical intervention, they will have some risk.

It's so important to keep that in mind. The only other thing I have to say about the mood section is there's another drug that's used specifically for bipolar, which is lithium carbonate, or science has called lithium. So it's literally like a lithium substance. This seems to have a stabilizing effect on mood. So bipolar, remember, has extremes like mania and depression.

Lithium helps to keep you stable. Any questions on antidepressants before you move on to antipsychotics? Yes?

The MAO dilutes the neurotransmitters in the axon diluter, right? Not dilutes. It's going to make it so there's more of that.

So inhibitor, MAO itself. Oh, yes, good. So yes, MAO, yes, dilutes how many neurotransmitters, like it eats some of them or whatever, like dissolves them. The MAO inhibitors stop that. So, yes.

Any other questions? Okay, the next category of drugs is antipsychotics. So psychosis, or psychotic conditions, is an umbrella that includes any conditions with hallucinations. delusions, other kinds of irrational propensities. So the type of psychosis we spent the most time talking about is schizophrenia.

That's the only one you really need to know. There are other more mild types of psychosis, but the type that's been most widely studied is schizophrenia. So you'll recall that there are some people who have argued that Too much dopamine transmission is involved in schizophrenia.

I don't know as much about that as I do about the serotonin theory of depression, but my impression is the evidence is stronger there for a connection between dopamine problems and schizophrenia. So as you can probably guess, antipsychotics reduce dopamine transmission. at least the main kinds.

Now one downside of this is it can produce a condition called tardive dyskinesia. This is a motor problem. So dopamine is involved in a number of different But one thing it's involved in is initiating voluntary movement.

And so, if you mess with the dopamine system, you can get this condition. This is somewhat similar to Parkinson's disease, which is also a motor condition. There's a kind of interesting relationship between schizophrenia and Parkinson's in that they're sort of opposites. So schizophrenia, there's some evidence that high dopamine is involved.

Parkinson's, we know for sure, has to do with low dopamine. They're dopaminergic. regions of the brain that are damaged in Parkinson's or that deteriorate in Parkinson's.

And so the treatment for Parkinson's is L-DOPA. You don't need to know that for the test, but it increases dopamine transmission. And it produces symptoms kind of like schizophrenia. That's kind of a side effect, is you go a little kooky.

You can have some schizophrenia-like symptoms. And then for schizophrenia, the treatment is to reduce dopamine transmission. And then you get this, which is kind of like Parkinson's. You don't need to know about the Parkinson's case. That's just to reinforce the point that there does seem to be this relationship between...

high dopamine and schizophrenia-like symptoms, and low dopamine and Parkinson's-like symptoms. So this is the name for a Parkinson's-like set of symptoms that results from taking antipsychotics. Any questions about that?

I have less to say about the antipsychotics, but any questions about that? conditions like schizophrenia. When you're on drug therapy, do you just like get prescribed for this new life or is it like... That's a good question.

So some people do need to be on them for life. I know it's the case that the antipsychotics target the positive symptoms more, so like the hallucinations, the delusions, and that those tend to be worse in your 20s and 30s. So maybe it's okay to go off them later in life if those aren't as severe. Don't quote me on that, though.

I'm not a clinician, but that's my recollection of that. Now as I say, these antipsychotics, the ones that target dopamine, are more effective for positive symptoms. You do not need to know this for the test, but there are a growing set of what are called atypical antipsychotics that work in other ways, and they tend to be more effective for the negative symptoms, like flat affect and things like that.

Another thing I'll mention that's not listed in the key terms, so don't worry about it, but there's also another category of drug that's used a lot for conditions, which is stimulants. Different types of stimulants, which increase brain activity, which speed the brain up. This is commonly used for ADHD.

which I always thought was kind of strange, because ADHD is like having too much energy and being too inattentive, but there is evidence that they produce some benefit. One conjecture could be that everything is kind of boring to them. They find nothing stimulating, so you give them some stimulants, and now they're able to pay attention, because they're able to find it more exciting.

That's a little bit conjectural, but there's some evidence that stimulants are effective for reducing ADHD symptoms. Though a very strong argument to be made that maybe they are also over-prescribed. Okay, that's the end of the section on drugs. The next type of intervention is a little savage.

I feel like we'll look back on this and be a little bit surprised that we ever did this. But it does produce benefits. I'm referring here to electroconvulsive therapy, or ECT. So, this is today most commonly used for treatment-resistant depression. It used to be used more broadly, but that is one issue for which the evidence is quite strong that this can be beneficial.

So by treatment-resistant, I mean you gave them an antidepressant, maybe you tried a different antidepressant, you tried some therapy, and the person is still suicidally depressed, so at serious risk of taking their own life. Obviously with the consent of the patient, what you do is you lie them down, you give them an anesthetic so you put them to sleep, you tie their limbs down so they don't hurt themselves. Although actually in the video I forget if they do. I have a video of this.

And then you run an electric... ...current through their brain to induce a brief seizure. And believe it or not, this is actually quite effective at reducing serious depressive symptoms. The main risk is temporary amnesia.

The person will sometimes have memory problems after. They are usually temporary, but that's the main risk. But again, if someone is at serious risk of killing themselves, sometimes you will do whatever is available.

Now, if you're squeamish, you can close your eyes and leave for a few minutes, but I actually have a video of this in action, so this is what ECT looks like. Okay, I'll stop there. Okay, so that's ECT. Another intervention that's even more rare is psychosurgery.

So this involves actual, you know, either cutting of different parts or even removal of small parts. One that used to be used a lot was the prefrontal lobotomy. This was used on very difficult... or even violent mental patients. It involved, and sorry it's kind of graphic, but sticking ice pick-like instruments beside the eyes and severing connections in the right parts of the frontal cortex, which often made patients more malleable and compliant.

Believe it or not, this was done to JFK's sister. She was a very serious, had very serious issues. Nowadays, we never do that. Yes? Oh, I didn't know that.

Okay, this person says Queen Elizabeth's sister. I don't know, but that wouldn't surprise me. So it was fairly widespread.

The book lists a few more minor examples that are still done today. You don't need to know the details, but in very extreme cases, this is sometimes used. The book has a discussion of deinstitutionalization.

This occurred in the 50s and 60s. There used to be significantly more long-term psychiatric hospitals where people would stay essentially for life. if they were too difficult to deal with or had too much trouble integrating into society. Many of them had severe schizophrenia. Following the development of psychiatric drugs like antipsychotics, it was thought that...

that maybe these people should be released and could be given long-term outpatient care. This was, I think it's fair to say, a profound failure. This led to a significant increase in homelessness. It turns out the medication was, in many cases, not sufficient to reintegrate them into society. I'm not saying the institutions were good.

They were obviously problematic. It's understandable why they were shut down. But there was not sufficient effort to successfully... reintegrating them, so many of these people wound up becoming homeless. And then the last pair of terms have to do with prevention.

So there's a growing move towards prevention. It's often a more cost-effective way of dealing with, or I guess not dealing with conditions, but stopping them before they arise. And the two types the book mentions are situation-focused prevention and competency-focused prevention.

Situation-focused prevention targets the environmental causes of psychiatric disorders, so poverty, crime, or child abuse, or things like lead in the water. That's one that's been widely studied. So getting rid of things like that is a way of preventing disorders from emerging. And competency-focused prevention is about teaching people coping mechanisms and resilience before they develop a disorder.

It's often good to target that towards people who are at risk. So that's the other kind of prevention. Okay, and that is the last term in this course.

Any questions? Okay, so I know some of you have been with me for two minutes. ...courses now, and I thought, do I have any, like, final words for this course, or for this pair of courses for some of you?

And one thing I'm in the mood to say after going through Chapter 17 is I would strongly encourage you to treat this book and psychology in general as a work in progress, right? This is why I encourage you all to not engage in self-diagnosis. psychology is a human activity and is therefore very fallible like anything is so this is not the final work this is a work in progress maybe some of you will contribute to furthering it along but don't take any of it as infallible That's one thing you discover as you get older, is that everything human is very fallible.

I have found that the closer I've gotten to the scientific process, in a way the more skeptical I've become of it. I think it's the best we have. I think science is the most reliable way of acquiring knowledge that we have, but it is still very much a human activity.

My mom had the same reaction. She was, uh, she got on the city council. She always loved politics. And the closer she got to it, the more she was like, wow, this is, like, very human. The people who don't study in high school grow up to run the world.

Those people get jobs when they grow up, so. And, uh, the same is true of science. Okay, so...

I'm mindful of the time. I actually don't think we'll have time to do the game unless we really rushed. Hopefully none of you are too devastated by this.

Any questions about anything in the course? The rest of the time is... is for you all, so any questions, because the final on Thursday is Q&A. Can you go over bipolar 1 and 2 and type 1 and 2 specifically?

Yes, so bipolar 1 and 2, so bipolar 1 is mania, so both 1 and 2 have depression, and that's the same, but bipolar 1 has full-blown mania, bipolar 2 only has hypo mania, so kind of like dying mania. Not quite full-blown. for type 1 and 2 schizophrenia type 1 is more positive symptoms delusions, hallucinations things like that type 2 is more of the negative symptoms like flat effect Additionally, Type 1 is often more sudden.

There are more people in the Type 1 umbrella who are perfectly normal, well-adjusted people, and then in their late teens or early 20s, they just lose their mind. Type 2 often emerges more gradually, and unfortunately is therefore associated with less likelihood of successful, a lower likelihood of successful treatment. Any other questions? Yes. Say again?

Oh, prevalence. You do not need to know the prevalence rates for different disorders. Kind of interesting information, but you do not need to memorize those. Yes.

You definitely need to know the symptoms of disorders. Those are good to know. Yes. Yeah, I would say all of that is fair game. So anything on the key terms, as usual, from chapters 2, 9, and 12 through 15, all of that is fair game.

So just a reminder. The final on Thursday is 70 multiple choice. 30 of them come from those first chapters.

Anything is fair game. And then 40 will come from chapter 16 and 17, 20 each. No written, there's no written on the final.

Now I will say, having said that, if you're going to be efficient, I would recommend focusing more on the big ideas from the early chapters. It's not to say that the details can't come up, but there's a better chance of the big ideas coming up. I think someone over here had their hand up first. I was in the same place.

Same place. Yep. Moving back to developmental... Yeah, all that's fair game.

Yeah. Any other questions? Anything in the book is fair game.

Questions? Yeah? What's the difference between exposure and response?

So technically, so the question was what's the difference between exposure response prevention and systematic desensitization? Technically, systematic desensitization falls under the umbrella of exposure response prevention. Reaction response prevention just means you expose them to something that induces anxiety normally and prevent them from doing what they normally do.

In the case of OCD, that means preventing the compulsive ritualistic behavior. In the case of a phobia, it means preventing the avoidance, preventing them from running away from it like they usually do. Systematic desensitization just means doing that slowly, step by step, starting at the bottom of the anxiety hierarchy and working your way up.

Can you go over the biomarkers for dementia or Alzheimer's? Yeah, Alzheimer's, there's just two. So there's two biomarkers for Alzheimer's, amyloid plaques and neurofibrillary tangles.

You don't need to know what they look like. Those are just two things you can see on the neurons of people with Alzheimer's. They're one of the things that distinguishes Alzheimer's from just ordinary dementia.

I just want to know if this definition is correct, but like this all therapy, like... Is the definition like it brings and just talks to immediate awareness so that like can be whole again? Not quite, it's thought therapy.

The word I would use is integration. You're trying to integrate your experiences into a whole. So people may feel scattered or disconnected in their memories or experiences.

Gestalt therapy, the goal of gestalt therapy is to bring them into a whole, to integrate them. Just like in perception, the gestalt psychologists study the ways in which we organize things into patterns or wholes. The therapist thought we should do something similar with our experiences and our methods.

I'm sorry, was the final exam weighted towards chapter 16 and 17 or 16 and 17? Yes, it is. So just as a shared number. So it's 70 questions, 20 of them from 16 and 20 from 17, and then 30 from all the others. other.

So it works out to, I think, like four or five per chapter. The reason for that, as I think I've mentioned, is for the other chapters, you're getting tested on them twice, in the final and in the other tests. So it works out to like seven or eight percent per chapter, as far as the multiple choice goes.

Yes, it's here on Thursday during normal class time. There's nothing during finals week. As of Thursday, you are all done.

That's the end. Yep. Yep, like everything I said today would be fair game. So yeah, like the names of the drugs, how they work, that's all fair game too.

No? For the personality disorders, I went through all of them mostly as a point of interest. The only two I would worry about are antisocial and bullying. Okay, so some people are leaving.

We'll call it there. If you have more questions, come and talk to me. I will see you all on Thursday. And if I don't see you after this course, good luck with your education.

Transcript for:Therapies, Treatments, and Exam Overview

Transcript for:
Therapies, Treatments, and Exam Overview