this is Professor Hoffman and this is the first in a series of videos to cover the content for topic eight in topic eight we'll be looking at central nervous system disorders and the medication classes that are used to treat those disorders so as we U move into this first video we're going to be looking at some of the background information um before we get into the classification so we're going to talk about how the CNS system functions in terms of the communication process between neurons and because that becomes really critical part of how we use medications that's essentially the part we're going to focus on with our medications when we're looking at these CNS disorders uh we'll go over some definitions of some common CNS disorders then as well and then from there we'll move on into some classification information so looking at communication within the central nervous system again remember central nervous system is made up of the brain and the spinal cord and all the neurons um that U are components of the brain and and the spinal cord you'll think back to anatomy and physiology and hopefully recall from that and from pathophysiology how nerves work essentially we're sending a action potential or an electrical charge down the length of the neuron or the axon the long band of it and that's an electrical activity that involves the movement of s sodium and pottassium uh so we do some changes in the polarity of the cell and when that action potential gets to the end of the cell at the terminal synapses it's going to cause the release of the neurotransmitters that that particular cell uh creates stores and then releases so what we're looking at in the brain is a communication between two nerve cells the originating nerve cell and then at the synapse or that space in between the cells um we're going to release neurotransmitters they are going to find receptor sites on the next nerve on the dendrites of the next nerve and that is going to start the whole process over again so the signal keeps getting passed on down uh from neuron to neuron until it gets to its sight of action so the key things on this process then at this uh Junction site is going to be the fact that neurotransmitters are released it's important to know that not every neuron releases the same neurotransmitters and on the dendrites or receiving side of nerve cells not all receptor sites are responsive to all neurotransmitters so we're going to be looking at very selective chemicals being released and also their actions on very selective receptor sites as we look using medications to deal with um some imbalances that may occur so as we look at the neurotransmitters that were're primarily concerned with when we're talking about central nervous system disorders so we're looking at issues such as anxiety depression um manic depressive or bipolar uh that those types of disorders we're really focused on some of the catacol amines or neurotransmitters that are basically amino acid based and the slide shows a list of the primary ones that we're looking at because the drugs that we're going to be using are going to be focused on um replacing these neurotransmitters supplementing them stimulating them that type thing we're going to look at a lot of agonistic behaviors in most of the situations so the first one the Gaba excuse me Gaba is an inhibitory neurotransmitter so that means when it's released it functions to sort of slow down responses on the receiving cell so it's going to be sort of a chill relaxation when we're looking at um impulses going on through uh so its effect is to again sort of a light emotional depression in a way or a chilling or calming effect so when we're looking at gabar Related Disorders if Gaba is low in its natural presence that is going to be related to instances of anxiety possibly seizures where we have a hyperactivity of cells uh man man Mania part of the bipolar uh process and issues with impulse control cuz normally Gaba would be again slowing the processes down and keeping everything calm so that will be one of the things we'll be looking at when we're talking about some Gaba responses serotonin you're probably more familiar with um at least in terms of drug class names when we talk about anti-depressants we talk about ssris we're talking about serotonin and increasing the amount of the availability of serotonin in that synapse so serotonin is going to have an impact on our sleep schedule it infects our temperature regulation because it ties a little bit into um our autonomic nervous system issues as well it's going to affect mood um libido just a number of areas there so again we'll look at serotonin particular when we're talking in the anti-depressant category dopamine is also one of the amino acids and also one of the camines out in the body and in your some of your classes your cardiac classes in particular cardiovascular you're going to talk about dopamine and its impact on uh the sympathetic nervous system uh and autonomic responses within the sympathetic nervous system in terms of blood pressure and heart rate and heart contractility in the brain though we're looking at dopamine is going to be linked to areas that control um motor uh motor responses and uh fine-tuning of motor responses it's also going to be active in areas of cognition so again in the central nervous system we're looking at a little bit different role for dopamine uh dopamine related issues are going to show up with ADHD schizophrenia and Parkinson's disease and particularly Parkinson is where we'll look at it quite a bit norepinephrine and epinephrine you'll remember from our earlier discussions on autonomic nervous system that they are the primary neurotransmitters for the sympathetic adrenergic system they're responsible for giving us the fight ORF flight responses out in the peripheral receptors in the brain um if we have a decrease in orine repine we're going to start seeing some depression of activity so that can also be emotional depression we're going to have a decrease in alertness and uh interest levels uh it's going to be involved with increases of norepinephrine epinephrine the stimulation we might get some anxiety and some panic attacks so again a little bit different responses than we saw out in the periphery under the autonomic nervous system things but still it's working as sort of a stimulant uh type neurotransmitter in the brain as well so if we have a lack of it we're going to see certain things we see an increase we're going to see some other behaviors so again those are some of the amino acids or catacol amines that we'll be referencing as we get into these drug classes and what their responsibilities are again just a real quick look at what happens in that synapse area between the original and the originating uh nerve uh terminal um terminal site and the receptor sites on the dendrites of the receiving nerve uh again receptor sites are specific to specific chemical are specific neurotransmitters um this uh terminal um of the ascending nerve is going to release specific chemicals not all neurons are going to release all the same chemicals not all receiving dendrites can receive all chemicals so that's that whole receptor site theory that we talked about earlier uh the other thing that's happening here is as those neurotransmitters are released into that space the goal is for them to the neurotransmitter to attach attached to those receptor sites there's going to be excess neurotransmitters released and we don't want the those to accumulate because we don't always want this stimulation happening and that's for the interaction between nerve and nerve and also out in the periphery when we have a reaction of nerve to muscle or nerve to other tissues so some of that excess neurotransmitter is just going to float away through the process of diffusion in the interstitial fluid so we're just going to have it moving away some of it is going to be picked back up by descending or original neuron on SES at that terminal that will re-uptake um the neurotransmitter so put it back into storage for reuse later and then some of the neurotransmitter is going to be degraded or broken down through the work of enzymes and since we're talking about catacol amines and amino acids that main enzyme that we're talking about is Mao the monoamine oxidase and again that's going to come up uh when we talk about anti-depressants with drugs that are going to be sort of block that action so the degradation or breakdown of some of the excess neurotransmitter getes a work of the enzyme and specifically Mao or monoamine oxidase as we look at uh some of the disorders I just want to go back and make sure I didn't jump here okay um the disorders that we're going to be looking at in terms of medication classes and treatment we're going to be looking at anxiety and this isn't just being nervous or being fearful of something this is um a response a central nervous system response where mood and behavior is Disturbed to the point that it interferes with ADLs uh we have a list of some of the uh manifestations or signs and symptoms that accompany man anxiety so we're looking at physical issues aches pain stomach and GI upset we're looking at the feeling of our heart racing the trembling sweating the difficulty concentrating some emotional um disturbances where it may be um agitated there may be crying that's just unprovoked it just happens so again anxiety we're not again just looking at that I feel a little nervous or I'm a little fearful about something a little bit um just sort of normal day-to-day we're talking about anxiety at the level that it actually starts impacting our ADLs so our treatment along with the pharmacological uh possibilities that we'll be talking about can also be non-pharmacological so this is where as we're looking at nursing interventions for our patients we want to be able to introduce such things as relaxation techniques want to encourage involvement in uh Psychotherapy some sort of counseling with a a trained counselor or trained trained therapist uh maybe helping people find support groups so there's a number of non-pharmacological interventions can help with this as well as the medication classes we'll be looking at another disorder we'll be looking at is depression and for depression it's not again it's not just a simple thing of I'm feeling down right now that sort of thing we're looking at clinical depression is going to consist of at least five of um the markers that are listed on the slide so it's just one or two that is not an unusual sensation to have and um won't say it will pass quickly but it's probably going to be manageable once we get this collection of five or more of these on a consistent basis again they're going to start interfering with our ability to function in um in our ADLs and be able to relate well so as we look through those um items again some of them are physical manifestations others are emotional some are um psychological type issues one of the key ones to really focus in on at the bottom of the list with depression suicidal ideation or suicide attempts are a very real threat of depression and we don't always have clear indications of where the individuals at unless we're paying really close attention so clinical depression is something to take very seriously and not just treat it as something that people are just in a down mood again along with medications there are some non-pharmacological treatments so Psychotherapy group therapy um and some different approaches along that way uh there's also electroconvulsive therapy it can be used in some cases uh by some providers so just a number of things but again with depression really want you to keep in mind that if we're sensing any issues of depression as we see um collection of these kind of manifestations we really want to focus in On A needs assessment or a risk assessment on the area of suicidal ideation uh because it is a very real um real possibility for individuals to get to that point bipolar disorders uh also known in the past as manic depressive uh they are drastic mood swings the manic phase is an extremely High hyperactivity very focused or seems to be very focused uh no need for Sleep uh just really on the go person people at the top of their game or at least they feel they are cycle through with extreme lows or depression periods so we have this movement back and forth and again it is drastic and they are extremely high or extremely low and so again we see some of the manifest manifestations we may see with these individuals so we need to sort of key into those we'll look at some medication um process we can use for those uh non-pharmacological treatments are going to be some of the same things that can be used with uh depression active therapy groups uh individual and group work uh the ECT or electr convulsive therapy might be an option so some other things but we'll also look at medications schizophrenia is a breakdown with our connect the individual's connection with reality so will usually first appear between the ages of 15 and 30 uh but then continue on and it can show up later in life as well so some of the common symptoms we're going to see um are just sort of withdrawal from reality a break with reality to where the individual is hearing voices where they're talking to themselves and not just the normal selft talk that we all we're all involved with but actual conversations uh some hallucinations of seeing things that aren't there starts to break with our needs in our current reality so some personal care neglect and over time just a decrease in available energy so we can break down the symptoms into three classifications one are the positive symptoms and this doesn't mean they're good symptoms uh it just means where we're seeing very active um manifestations going on so this would include the delusions these can be delusions of persecution everybody's out to get me they can be delusions of grandiosity where I am the greatest thing going and nobody can touch me that sort can be a delusion of reference where people are talking about me it's not just the persecution but in individual sees in things that are in print in conversations and they always see a link back to themselves somehow it's tied to them so again these are breaks with reality that involve this altered um conception or perception of reality on the negative symptoms then we're seeing where we start withdrawing um mentally emotionally and physically so we have the apathy a lack of motiv Mo lack of motivation uh Speech even becomes more brief we start avoiding relationships so these would be the kinds of things that go into a negative be classified as negative symptoms then we're going to see changes in the cognitive functioning so poor decision making loss of memory the distracted difficulty focusing and we tie that back in with the delusions um and some of the negative symptoms we start seeing this picture of an individual pulling more and more away from reality as the rest of the world recognizes it into their own world treatment goal for schizophrenia is really going to be symptom control it is a disorder it is a disease um not necessarily curable but the goal is to manage the symptoms keep the individual uh in contact with reality um as it exists and get and moving out of that world or being able to live in the real world and understand what's going on in their mind as well so again whether it's pharmacological or non-pharmacological we're really going to be focusing on that symptom management symptom control another CNS disorder which gets in the area of hyperactivity or hyper responsiveness of nerve cells would be ADH D so the we see inability to concentrate difficulties with self-control difficult emotional control it's because some hyperactive responses going on in the brain in the areas that help with those um cognitive functions a seizures uh again or a CNS disorder a seizure is going to be caused is due to abnormal neuron activity in the brain basically we they are hyper excitable so we have massive firing of multiple neurons and not in a coordinated fashion can sort of relate it to if you're more familiar comfortable with cardiac function when we talk about atrial fibrillation and look at the conduction system in the heart where uh The Atrium have multiple sites that are firing off impulses and the atrium just sort of go into a quivering same thing can happened in the ventricles so sort of think of seizures as being the same kind of thing up in the brain we have multiple areas of neur neurons that have been become hyp um excitable so they start fir firing off and we start losing that focus and purposeful movement and flow of signals uh outwardly how we're going to see that so again the seizures are what H is happening in the brain outwardly what we may see are the um man physical manifestations when the motor S motor neurons are affected so the signals going out to the we're going to start seeing SE convulsions so what we normally call a seizure are visible convulsions they're representing the seizure misfiring of uh neurons in the brain so with the motor symptoms we have the um jerking type motion the tensor rigid muscles that gives us aonic clonic action muscles may not get signals so they're going to be weak there may be some twitching um maybe some epileptic spasms which again it's just just this irregular response of the motors because they're getting mixed signals or multiple signals that are not in um not being purposeful within the brain we're going to see some non-motor symptoms so this seizure activity in the brain is also going to impact our ability to interpret signals coming back so there's going to be changes in sensation we're going to have some cognitive and emotional changes if those parts of the brains are the ones have the sections that are misfiring uh some classifications when we're looking at seizures a simple partial or simple well we'll start with partial um par IAL seizure is usually focused in one area one hemisphere of the brain and one particular areas so the symptoms we're going to see are we really tied into what area of the brain is involved so if it involves motor skill and I'm having seizure activity in the right hemisphere I'm probably going to see motor uh evidence on the left side of my body of either some jerking tonic clonic activities twitching some of that type of thing a partial uh simple partial is just involving that a little bit of sensory going out but then also activity going back out on the motor signals complex partial seizures um start involving some cognitive impairment as well um and it may actually be focused more in the brain so we may or may not see the motor activity but it's still a partial seizure a generalized seizure then is going to involve um this misfiring happening in both hemispheres of the brain and on a wider scale so we're going to see much more many more body parts involved in the manifestations if they're convulsion type activities the tonic clonic activities we're also going to be seeing um those internal emotional and cognitive changes happening as well status epilepticus is a condition where the seizures either start and maintain as a one constant seizure activity for more than 20 minutes or it's a series of repetitive seizures uh coming so quickly that there's no time for the body to recover in between so status epilepticus is using a lot of energy it's putting a lot of strain on the neurons in the brain it is beginning to cause injury to those cells so status epilepticus is a life-threatening situation seizures the simple seizures um even the generalized seizures if they're very short duration um are not necessarily lifethreatening in and of themselves status epilepticus can be it's get it's going potentially lead to irreversible brain injury and it can be associated with a high rate of mortality so we this is one we're going to want it to get into and treat very quickly so you'll talk about that in your clinical courses uh Critical Care area especially uh then the last disorder that we'll look at classifications for is Parkinson disease Parkinson disease is a an a chronic progressive disorder it is focused on a breakdown of the myelin or that insulating sheath that's on the axons or the long fibers of the neurons and because that is broken down we get a very weak um action potential sent down that neuron so we get very low stimulation beyond that point so we're going to see movement imperatives primarily involve the section of the brain that works on the fine-tuning of our movements um if you think back to anatomy and physiology and pathophysiology would have talked about um the parameter uh nervous system which is our coming from our motor sections of the cortex of our brain and telling us to make the gr our gross motor movements the extra paramal part of the system is deep in the brain located around the thalamus U and this is where all the fine tuning goes this is the part that's affected by Parkinson's disease the neurons coming in and out of that area uh start breaking down they start having weaker signals um and we start getting the symptoms then so we're going to see some Tremors at rest rinia which is just very slow movement with the gate disturbance is going to be sort of a shuffling gate the individuals not really going to lift their feet as the diagram shows as it progresses there's going to be that stooped stooped posture um and it's going to affect moods there's going to be some mood swings going along with it too um from a neurotransmitter perspective it seems to be really tied into the availability of dopamine and the ability of dopamine to function within that extra parameter environment so we look at the drug classes uh for treatment of Parkinson's that's really where we'll be focusing our um attention so that's the background information uh in the next uh several videos we'll talk about these individual disorders in terms of drug classifications that we'll use in their pharmacological treatment