In this video I begin describing biomedical approaches to mental illness in more detail and focus on psychopharmacology. I describe some of the main mechanisms of antipsychotic, anti-anxiety, and antidepressant medications, along with the uses and potential side effects of these medications. Disclaimer: This channel is for educational purposes only and is not intended as medical advice for the diagnosis or treatment of psychological disorders.
Tardive Dyskinesia example video here.
Video Transcript
Hi, I’m Michael Corayer and this is Psych Exam Review. In the previous two videos, we looked at a number of approaches to psychotherapy for treating mental illness. And in this video, and the next video, we’re going to turn our attention to biomedical interventions for treating mental illness.
And we can start with one of the earliest known biomedical interventions. And this is a practice known as trephining or trepanning. And this can be seen in a number of cultures and it’s estimated to date back to about 6000 BC. And this practice involved drilling holes in the skull. And this was often related to beliefs that this would release demons or evil spirits that were tormenting the person. And here we can see a skull that has been trepanned and we can see these holes in the skull. And it might surprise you to learn that this procedure was not always deadly. Of course, it probably was in many cases, but people did survive this procedure. And the way that we know that is we can see bone growth around these sites. And so that suggests that the person stayed alive for quite some time and began to heal after this procedure was conducted.
Now it might not surprise you to learn that trepanning is no longer practiced today. So in this video, we’re going to mostly focus on the use of drug treatments to try to influence emotions, thoughts and behaviors. And this is what we can call psychopharmacology. And it’s important to note at the beginning that none of the drugs I’m going to talk about in this video are magic bullets. These are not cures for these symptoms or for these disorders. In part, this is because psychiatric illnesses are incredibly complex and most of the drugs work by affecting some neurotransmitter or some receptor site. And this means that it will affect many different kinds of those receptor sites. So one drug will affect many different receptors and then those many receptors will affect many different behaviors or many different other outcomes in the body. And so for this reason, we don’t have a simple 1 to 1 solution. We say OK, this drug will cause this specific effect and will cure all the symptoms. And another result of this, beyond the fact that we don’t have these magic bullet cures, is that we often see a number of negative side effects associated with the use of these drugs.
And I’m also going to talk about a number of the drug names in these videos. I’m going to give you examples, for most introductory courses you wouldn’t be expected to know the names of the chemical structures and also the brand names of these drugs. But I’m going to mention them some of them, because you might have heard of some of these drugs before and you might not know exactly what they are. So by mentioning them you might recognize some of these names or if you live in a place like the United States where there’s direct consumer marketing for pharmaceuticals, then you might actually recognize from TV commercials were advertisements, some of these drugs that are described okay.
So we’ll start with antipsychotic medications, these can also be called neuroleptics, and these are drugs that are frequently used to treat schizophrenia. And the very first antipsychotic drug resulted from the work on an antihistamine drug and this led to the creation in 1951 of a drug called chlorpromazine or Thorazine. And it was soon followed by some other neuroleptic drugs, including thioridazine or Mellaril and haloperidol or Haldol. And these drugs often caused a sense of euphoria and docility in the patients, so they became much easier to manage in mental institutions.
And one result of this was what’s known as deinstitutionalization. This occurred in the 1950s and 60s where millions of patients were released from mental institutions. They were given these neuroleptic drugs, which reduced a number of their symptoms and made them much more docile and easier to manage. And as a result of this deinstitutionalization, mental institutions saw a reduction by about two thirds in the total number of patients that were institutionalized. And it’s important to note that release is not synonymous with cure. So this is not necessarily a good thing in many ways. This was a disaster because people were released who didn’t really have the means or ability to care for themselves, or they didn’t continue taking their medications and their symptoms returned. And a result of this deinstitutionalization was unemployment and often homelessness for people who had previously been institutionalized.
Now, the main mechanism of these antipsychotic drugs is that they block the neurotransmitter dopamine. And this is associated with what’s known as the dopamine hypothesis of schizophrenia, which suggests that these symptoms of schizophrenia result from excessively high levels of dopamine in certain brain areas. And so by blocking some of that dopamine, we’re able to reduce some of those symptoms. And this can be effective, particularly for reducing the positive symptoms of schizophrenia, so things like delusional beliefs or hallucinations. But it’s not so effective for reducing the negative symptoms like social withdrawal and these drugs also come with a number of side effects. These include sluggishness, tremors and twitches, and one particular tremor problem that’s known as tardive dyskinesia. And this is a type of facial tic and repetitive gestures, particularly the mouth that come as a side effect of these antipsychotic drugs. And I’ll post a link in the video description where you can see some patients suffering from this tardive dyskinesia. Another side effect is weight gain. And this means that patients taking these drugs are at greater risk for other health problems like obesity and diabetes. And another side effect is what’s known as akathisia. And this is the Greek for “unable to sit”. And it’s a kind of painful restlessness and agitation that can occur throughout their whole body. And this often leads them to pace around the room in an attempt to try to reduce some of this agitation. And it can be very, very painful for these patients. And in some cases, it’s so severe that patients will refuse treatment or refuse to take the medications because they want to avoid this particular side effect.
Now, there are newer drugs for treating schizophrenia and these are referred to as atypical antipsychotics and examples of these drugs are clozapine or Clozaril, risperidone or Risperdal and olanzapine or Zyprexa. And these drugs also influence the serotonin systems in addition to the dopamine system that the typical antipsychotics influence.
OK, next we’ll take a look at some anti-anxiety medications. And these can also be referred to as anxiolytics. And these are drugs that reduce anxiety. And they can also be used to help extinguish learned fears. So in the previous video, I talked about behavioral treatments like exposure therapy for anxiety disorders and sometimes these behavioral techniques are combined with medications. So people might take an anti-anxiety drug prior to their exposure therapy session in an attempt to help them to extinguish the learned fears more quickly by reducing their anxiety. And the main class of anti anxiety medications are benzodiazepines. And these are drugs that mostly influence the GABA system. And a GABA is a neurotransmitter, gamma amino butyric acid, and the main way that these drugs work is they reduce heart rate and thus help to reduce feelings of anxiety. And these take effect very quickly, so this reduction in heart rate occurs within minutes of taking the drugs.
Now there are a number of side effects associated with these drugs. And these include drowsiness and problems with memory and coordination. And these drugs can also be very dangerous if combined with alcohol. So occasionally people do take these drugs recreationally and this can be especially dangerous if they’re also drinking. And these drugs also carry a risk of addiction, dependence, and withdrawal. And so in the case of withdrawal, what we see is when people stop taking these anti-anxiety medications, they feel heightened anxiety. And some examples of these benzodiazepines are diazepam sold as Valium, lorazepam or Ativan, and alprazolam or Xanax. And one thing we might wonder when we think about these anti-anxiety medications is whether they’re really treating anxiety. Certainly they’re reducing the symptoms, but we might wonder if it’s just masking those symptoms, because the patients aren’t necessarily learning how to cope with their anxiety. And all they’re really doing is sort of suppressing their heart rate by taking these medications. And so we might wonder, is this really a treatment, or is it just a way of hiding the negative symptoms, the elevated heart rate, the feelings of anxiety, without actually really changing the person?
And lastly, we can look at or sorry, not lastly, but next we can look at antidepressant medications. And these are the most commonly prescribed psychiatric medications. And in fact, they’re one of the most commonly prescribed medications in general, in the United States. And so the first antidepressant medication actually resulted from a drug that was designed to treat tuberculosis. And this was a drug called iproniazid. And one of the side effects of this drug was that it caused people to feel euphoric. And this led to the suggestion that maybe this could be used to treat people who are depressed. And the reason that it had this effect of euphoria is that it’s a monoamine oxidase inhibitor. And so monoamine oxidase is an enzyme in the body that breaks down monoamines. And monoamines include the neurotransmitters, serotonin, dopamine and norepinephrine. And so the basic idea is these monoamine oxidase inhibitors prevent this enzyme, they inhibit it from doing its job of breaking down these neurotransmitters. And as a result, you get greater activity of these neurotransmitters than you would have if the enzyme were doing its job.
Now this results in side effects when you’re preventing this enzyme from doing its job. And these include dizziness and reduced libido. And there’s also the possibility of a dangerous interaction with an amine called tyramine. And so this is a substance that you find in certain fermented foods, things like cheese and certain meats. And what this means is the person taking these monoamine oxidase inhibitors has to follow a very strict diet in order to avoid this interaction with tyramine, which can lead to a hypertensive crisis, which is a dangerously elevated blood pressure. Okay, so for that reason, monoamine oxidase inhibitors are not commonly prescribed today.
They were replaced by another sort of generation of antidepressants known as tricyclic antidepressants. And the tricyclic refers to their three ringed chemical structure. And these include the drugs imipramine or Tofranil and amitriptyline, or Elavil. And these drugs work by blocking the reuptake of serotonin and norepinephrine at the synapse. So you might recall from the unit on biology that after a neurotransmitter is released, some of it is taken back into the presynaptic neuron. This is a process called reuptake. And so by blocking that reuptake, the neurotransmitter can stay in the synapse longer. And so that’s essentially what these tricyclic antidepressants are doing. And this, these drugs, also have side effects associated with them, which include dry mouth, blurred vision, skin rash and elevated heart rate. And another risk of these drugs is that there can be symptoms of withdrawal when the patient stops taking them. And this can result in anxiety, headache, nausea, insomnia and motor disturbances. And for this reason, the patients have to be gradually weaned off of these drugs. They can’t stop suddenly. And this is another reason why these drugs are actually not so commonly prescribed today.
But this success of some of these early drugs in treating depression led to what was known as the catecholamine hypothesis. Catecholamines refers to these groups of neurotransmitters, including epinephrine, norepinephrine and dopamine. And this was gradually refined to focus particularly on serotonin. This is known as the serotonin hypothesis of depression, that depressed mood results from disturbance to the serotonin system. And so by regulating the serotonin system, we can help to improve mood.
And this brings us to the most commonly prescribed type of antidepressants today. And these are the SSRI’s, or selective serotonin reuptake inhibitors. And so some common examples of SSRIs are fluoxetine, sold as Prozac, citalopram, sold as Celexa, paroxetine or Paxil and sertraline, or Zoloft. And these are drugs that you’ve probably heard of, or even seen television commercials for. And these essentially work by blocking the reuptake of serotonin, allowing it to stay in the synapse longer and therefore be more likely to find its receptors. And this will influence the activity of the serotonin pathways. And the side effects of these drugs include nausea, agitation and sexual dysfunction.
And there are more recent antidepressants that are not SSRIs, that are what are called atypical antidepressants. And these influence the norepinephrine and dopamine pathways. And so examples of these drugs are venlafaxine or Effexor, nefazodone or Serzone, and bupropion or Wellbutrin. And it’s an important note that even though these drugs are so commonly prescribed, these SSRIs, as well as these atypical antidepressants, their mechanisms are not fully understood.
And one of the ways that we can see that is that when I describe this process of blocking reuptake, it seems very simple on a chemical level. You block the reuptake, the neurotransmitter has more time in the synaptic cleft to do its job. And you know that somehow relates to the person’s mood. But what we see is that process happens immediately after taking the drug. And yet symptoms often don’t get better for several weeks after starting the treatment. And so if somebody starts taking a drug like Prozac, their synaptic activity is being influenced almost immediately, and yet they won’t start feeling better for maybe two or three weeks. And so this suggests it’s not a simple imbalance or deficiency of a neurotransmitter. In fact this chemical imbalanced idea that most people are probably familiar with, they’ve heard of depression described as a chemical imbalance is not really accurate, because if it were just an imbalance, you could just put in some more of this neurotransmitter or increase its activity and that would solve all the problems. But that’s not the case.
Instead, it’s suggested that the reuptake, the blocking of the reuptake, may somehow change these pathways, but that change will take time. So that process of neuroadaptation where the body will change in response to chemicals or drugs that are present, this might actually be what’s reducing the depressed mood. And another suggestion is that these drugs somehow influence neurogenesis, that’s the creation of new neurons, the growth of new neurons, particularly in the hippocampus. And so it might be the case that these SSRI’s are improving neurogenesis and that that’s actually more responsible for the improvements in mood and something we’ll come back to in a future video is the role of exercise on improving symptoms of depression. And exercise may be something that also is improving or increasing neurogenesis in the hippocampus. But we’ll come back to that in a future video.
Now, it’s also interesting to note that these antidepressant drugs are used for a number of other disorders as well. This is part of the reason why they’re so highly prescribed and they can be used for treating anxiety disorders, eating disorders, obsessive compulsive disorder, attention deficit hyperactivity disorder, as well as premenstrual dysphoric disorder, and also for smoking cessation. And it’s interesting to note that when these antidepressants are used for some of these other illnesses, or disorders that aren’t so directly associated with depression, like smoking cessation, the drug companies often use different names. They brand them differently. The pills look different, but they’re the same drug. And this is a way of trying to separate some of the associations people might have with a certain drug for depression from something like their premenstrual dysphoric disorders. So in the case of PDD, there’s a drug called Seraphim that is prescribed. And this is actually just Prozac under a different name. And similarly, the smoking cessation drug, Zyban, is actually Wellbutrin, but these different names are to try to change some of those associations people might have. And this maybe is influencing things like the placebo effect and the success people might have with these drugs.
Okay, lastly, we’ll take a look at some bipolar medications, and you might expect, given that antidepressants are used for so many other disorders, anxiety disorders, eating disorders, that they would also be used for bipolar disorder. Because, you know, a main symptom of bipolar disorder is depressive episodes and the diagnostic criteria for those depressive episodes are identical with major depressive disorder. And yet antidepressants are not used to treat bipolar disorder. The reason for this is that these drugs can actually trigger manic episodes. So they are generally to be avoided for somebody suffering from bipolar disorder. And instead, the main drug for treating bipolar disorders is lithium. And this is what’s known as a mood stabilizer. And another drug that is occasionally used is Valproate, and this is an anti-convulsive drug that can help to reduce some symptoms of bipolar disorder.
But the main treatment is lithium. And for about 60 to 70% of people suffering from bipolar disorder, they will respond to lithium and it will help to prevent manic episodes and it can also reduce the severity of their depressive episodes and reduce the risk of suicide. But, of course, this comes with a number of side effects as all the drugs we’ve seen have. And in this case, lithium is associated with nausea and weight gain. And it’s also important for the patient to carefully monitor their dosage of lithium because high levels can lead to kidney and thyroid dysfunction. And it’s also a case that lithium is teratogenic, which means that it can harm the development of a fetus. So if a woman is pregnant, who suffers from bipolar disorder, she can’t continue taking lithium during her pregnancy.
Okay, so those are some of the main categories of pharmaceutical drugs that are used to treat mental illness. And the next video will take a look at some other biomedical interventions. And then we’ll also think about how we can evaluate the effectiveness of different treatments. I hope you found this helpful, if so, please like the video and subscribe to the channel for more. Thanks for watching!
