0:00 In this video, we're going to talk about psychosis. 0:08 Now, psychosis encompasses a variety of diseases, including that of 0:13 schizophrenia. 0:15 Psychosis is loss of contact with reality. 0:17 12 to 23% of people experience a psychotic symptom at some point in their lives 0:23 , but 0:23 less than 4% meet the criteria for a psychotic disorder, and this is, of course 0:30 , in a DSM. 0:33 So what features do we see in someone who has psychosis? 0:35 Well, there are four cardinal features, or clinical manifestations. 0:41 These are delusions, hallucinations, thought disorders, agitation, and 0:47 aggression. 0:48 So what do these mean? 0:49 Well, let's look at delusions, hallucinations, and thought disorder, or 0:53 thought disorganization in more detail. 0:57 So delusions are defined as strongly held force relief that are not typical of 1:05 the person's 1:05 background or culture. 1:08 Further, delusions can be categorized based on its plausibility. 1:12 So delusions can be bizarre, or delusions can be non-bizarre. 1:17 A bizarre delusion, an example of that is the person thinks that their family 1:22 member has 1:23 been replaced by someone else. 1:27 And then a non-bizarre delusion is something like the person thinks that their 1:35 partner 1:35 is cheating on them, so it's not as bizarre, if that makes any sense. 1:41 And then you have hallucinations. 1:42 Now, hallucinations is defined as a wakeful sensory experience of contents that 1:47 is not 1:48 actually present. 1:49 And sometimes hallucinations and illusions are actually used interchangeably, 1:54 but 1:54 they're different because, again, hallucinations is a wakeful sensory 2:00 experience of content 2:02 that is actually not present. 2:04 And illusion is actually a distortion or misinterpretation of real sensory 2:12 stimuli. 2:13 And then you have thought disorganization. 2:15 And these are just disorganized patterns of speech, and they include a lot of 2:21 things, 2:21 but I kind of go into it in detail, but these are just some of them. 2:28 Alargia, thought-blocking, loosening of association, tangentiality, clanging, 2:33 word salad, and perseveration. 2:37 So we see these things in a person who has psychosis, but not everything. 2:43 And psychosis occurs or is caused by a primary disease or a secondary disease. 2:51 So what I mean by this is primary disease is more of a mental illness, and 2:57 secondary is 2:58 attributed to an underlying disease. 3:01 So some illnesses with psychosis, so the primary disease, include schizophrenia 3:08 , schizo-freniform 3:10 disorder, schizo-affective disorder, delusional disorder, schizo-tial 3:17 personality disorder, 3:20 and then we have substance abuse. 3:21 So these are the primary illnesses with psychosis. 3:25 Then you have secondary psychosis, and this is, again, attributed to an 3:29 underlying disease, 3:30 such as thyroid disease, adrenal disease, hepatic and solopathy, Wilson's 3:36 disease, Alzheimer's 3:38 disease, Huntington's disease, and stroke. 3:43 So what changes actually occur in the brain to make someone experience 3:49 psychosis? 3:50 So now let's zoom into the brain and look at the areas affected in a person's 3:54 psychosis. 3:55 So the two main areas I want to introduce, the limbic system and the frontal 4:00 cortex. 4:00 And the actual names, I'll just use abbreviations first. 4:04 These are in the limbic system, the VTA and the NAC. 4:09 And then you have the prefrontal cortex, PFC here. 4:13 And the two, I guess you can say, neuronal pathways affected in someone who has 4:19 psychosis, 4:20 with a mesocortical pathway, which is a pathway from the VTA here to the 4:25 prefrontal cortex. 4:26 And then the other pathway that is affected is the mesolimbic pathway. 4:30 So that's between the VTA and the NAC. 4:34 So let's just go to a bit more detail, beginning with the mesolimbic pathway. 4:39 So here is the NAC, known as a nucleus accumbens. 4:44 And here is a neuron that travels from the VTA to the NAC, the nucleus accumb 4:55 ens. 4:56 So 60% of neurons in the VTA are dopaminergic, and it is controlled by GABA-n 5:02 ergic neurons. 5:03 So usually there's GABA neurons that are controlling this neuron I drew here. 5:09 So this neuron is a dopaminergic neuron, which will release dopamine to the 5:13 nucleus accumbens. 5:15 Now in psychosis, you actually have this neuron releasing so much dopamine. 5:21 So if we were to look into the synapse between these two, we can see here is 5:26 the NAC, the 5:27 neuron of the NAC. 5:28 And then here is the neuron of the VTA, and the VTA neuron is releasing 5:34 dopamine DA. 5:35 And in psychosis, there's a lot of dopamine being released in the synaptic cle 5:40 ft. 5:40 With a lot of dopamine in the synaptic cleft, it will bind onto the receptors, 5:45 the D2 receptors, 5:46 the dopamine 2 receptors. 5:48 And as a result, the people will have the positive symptoms. 5:57 And these include delusions and hallucinations. 6:00 So positive symptoms is essentially something that is exacerbated in the person 6:06 . 6:06 So a person who has psychosis has positive and negative symptoms, as we will 6:10 soon find 6:11 out. 6:12 And so the positive symptoms are delusions and hallucinations, and it is 6:16 attributed to the 6:20 increase in dopamine between the VTA and the NAC. 6:25 So what happens in the mesocortical pathway? 6:27 Well, the mesocortical pathway is again between the VTA and the prefrontal 6:32 cortex, the PFC. 6:34 So this neuron is traveling from the VTA to the PFC. 6:38 And this neuron, as we learned, is a dopaminergic neurons, because 60%, most of 6:43 it are dopaminergic 6:44 neurons. 6:46 So this neuron will release dopamine into the synaptic cleft, and the dopamine 6:51 will bind 6:51 onto the prefrontal cortex. 6:53 However, in the mesocortical pathway, we actually have low amounts of dopamine 7:00 in a person with 7:01 psychosis. 7:02 So if we were to zoom into this area, and someone who has psychosis, here I'm 7:05 drawing 7:06 the VTA and the PFC, the connection, you actually have low amounts of dopamine 7:12 being 7:12 produced and secreted. 7:15 And so there's low amounts that will bind onto the receptors here. 7:19 The receptors here are D1 receptors, unlike the D2 receptors in the mesolimbic 7:26 pathway. 7:28 And so as a result of this decrease in dopamine in the mesocortical pathway, 7:33 the person develops 7:35 negative symptoms. 7:37 And the negative symptoms include ovulation and a flattering effect. 7:45 So essentially, it's decreasing social abilities and sort of sadness. 7:53 So I hope those changes made sense in a person who has psychosis. 7:57 So you have, again, changes in the mesolimbic pathway, and then you have 8:01 changes in the 8:02 mesocortical pathway. 8:04 So what are the treatments for someone who has psychosis? 8:09 Essentially, all antipsychotics are dopamine 2 antagonist. 8:16 Now these dopamine 2 antagonists can be classified as first-generation, known 8:23 as typical. 8:25 And this just means that they were made first. 8:27 And then you have second-generation, which is atypical. 8:33 And second-generation can be classified further because most of the second- 8:39 generation are D2 8:41 antagonists. 8:42 But they also can target serotonin receptors. 8:46 So they could be serotonin 2 antagonists and serotonin 1 agonists. 8:52 And don't be confused by all that. 8:55 Just know that there are two types of antipsychotics. 8:58 There are first-generation and second-generation. 9:01 And the second-generation targets other receptors as well, which are the 9:05 serotonin receptors. 9:06 So let's look at where these antipsychotics will have an effect. 9:10 Remember the mesolimbic pathway? 9:12 We have an increase in dopamine in the synaptic cleft here and that they will 9:18 bind to D2 receptors. 9:19 So essentially, the antipsychotics will inhibit the D2 receptors and thus 9:24 inhibit or stop the 9:25 positive symptoms coming alive. 9:29 And then some antipsychotics can actually work on inhibiting dopamine being 9:33 released into 9:33 the synaptic cleft here as well. 9:35 So I hope you enjoyed this video. 9:36 I hope it made sense. 9:37 Thank you.
