Basal Ganglia | Structure Function | Neuroanatomy | Dr Najeeb

so today we are going to talk about the motor functions of basal ganglia it means there are some other functions which are other than the water right even though average world only talked about the motor functions motor functions of basal ganglia actually this is misnomer right it should not be called ganglia because by definition ganglia on this collection of cell bodies in neuronal cell bodies outside the central nervous system but of course be willingly are present within the central nervous system so now they are called basal nuclei how do you define nuclei how do you define nuclei oh you are going to she says is that nuclei are collections of cell bodies in the central nervous system surrounded by the white matter because cortex is also collections of cell body is there right so basal ganglia are actually basal nuclei right why we don't call them ganglia because ganglia are by definition collections of cell bodies of neurons outside the central nervous system but as basal ganglia present within the central nervous system so the name is now replaced by basal nuclei right now exactly what they are right these are the masses of gray matter at the base of cerebral hemisphere right these are messes of gray matter at the base of cerebral hemispheres right so let me draw a diagram and show you how where exactly they are present right let's pose here cerebral hemisphere midbrain of course poorer then metal a spinal cord now you must be knowing that here are first of all just above the midbrain what are these two structures which are bilateral present adjacent to each other yes this is a solemn i right these are thalamus and just lateral to the thalamus lateral to the thalamus the messes of gray matter here on bilaterally on both sides right these are to Talam I on the sides of that there are two more masses of gray matter and in between them of course what is here this is white matter right this bundle of white matter is called internal capsule there's good now there are my let's make a little kitchen here just remember these are two eggs hello my are like eggs and on this side these are two pieces of cheese right there is a little kitchen here these are two ads and on the side what are these these are two cheese pieces is the right okay now I will bring this kitchen out because I have to draw some other important things you always understand whenever there is kitchen at night there are rats also so there will be some rats also here let's say that here I put this egg which is column i right and on the side these are cheese pieces right and of course all of them are gray matter right now on the thalamus on the AG special type of rat is sitting there there is a rat sitting over here right and here is the head of the rat right this is the head of the red here is the body of the rat and here is going to be the tail of the rat now what is this that this this is a c-shaped mass of gray matter or because it is embedded within deep in central of a system C shaped nucleus right and this is panel bilaterally when we say this is present bilaterally now this green colored structure this is called not red what we call it yes quadrate nucleus what is it quadrate nucleus so this is our quadrate nucleus right am i close now we can imagine like this the one of you can come here oh I have to take an example okay but you are so tall you'll make me look even shorter but anyway this is life you know wow he is coming in camera or not he's encounter okay just make it like this look yeah in front of them so what is this these are two thala my is their right and what are these on the side these were two eggs and these are two cheese pieces this cheese piece in this cheese pieces basically masses of gray matter this mass of gray matter and this mass of gray matter which is cheese piece this is basically called lenta from nucleus so there are hella my on the sides we have what are these lengthy form nuclei and then what is happening rat is sitting on the thalamus here interior part of the rat head of the red going like this over the thalamus behind the thalamus and then tail is coming under it so what happened rat is sitting in this arrangement and here also it is sitting like that arrangement now this rat structure is basically quadrate nucleus so what structure we arranged in here tell mi on the side of the phthalimide era lenta form nuclei right on the hello my there is quadrate nucleus if you follow it anteriorly to move forward and laterally and head of the quartet will be trying to approach yes geez red love to lick the cheese so right head of the caudate then body is accorded overhead and then tail of the caudate going from here is that right thank you now in this diagram when we see structure like this is the right now in between these structures there the gap here and there is a gap here is that right what is present in this gap yes you don't know it you must be knowing Scott internal cap so what about you it's very easy to understand here is cheese here is egg here is the rag and here is some yes what is this salad salad pieces here and this salad pieces these blue structure is basically bundle of axons of course white matter right what are these these are bundled off and lawns which is passing through this gap they are descending quantico cortical fibers are going down and there are other fibers which are going up so what is really there what we really see that the messes of gray matter having a c-shape gap and through this gap white metals going up and down this compressed white matter in this gap this is called internal capsule now the question is that why it is called internal capsule why it is called internal capsule because there must be something external capsule also actually there is some white matter which is also present over here right here and here so when initially when neurologists made section in this area what did they see I will draw it here now this are that here is thalamus ulemas right they found there was another mass of gray matter which which we will call him we were calling lanta form nucleus and when they are making a section head of the caudate was somewhere yes here and here this was the right you know it's cut section of the reactors we mean now is that right now actually when they made a section here white matter which was going up and down that was pressed between these structures is that right so white matter was going up and down in between these messes of gray matter is that right and this was this white matter was having another white matter outside this structure right now this was looking like a lens so they called lenta from nucleus this piece of cheese was lenta from nucleus and this gray lenta from nucleus was apparently surrounded by white matter inside as well as outside so they called it that this lenta from nucleus is in a white cap Sol this was considered internal capsule and this was considered external capsule is that right so what did internal capsule internal capsule is just collection of lot of exons bundle going up and down right between the thalamus and lenta from nucleus posteriorly and interiorly between the caudate head and lenta from nucleus it's not right but there is external capsule also which is laterally to the what is the structure lateral to the land of ham nucleus then any question up to this is it clear now if you go more laterally they found a little thin piece off gray matter here right what is this piece of grey matter called let's start from the center what was this this was hell am I is that right laterally you move what is this here internal capsule more laterally you move there is a lengthy form nucleus is the right more laterally you move what is it external capsule more laterally you move what is it claustrum the structure is called loss from and then there is another thin capsule here can white matter right and this is called of course if this is internal capsule this is internal capsule this is external capsule right what should be this one now extreme capsule very good this is called extreme capsule is that right these basic structure at the base of the brain are clear there's no problem with this is there right now I will draw these structures here we go back to our original diagram which we started our lecture with it that they were phthalimide and they were internal capsule laterally to that they have a lengthy form nucleus and then what is here justplease external capsule and what is here very thin grey matter yes claustrum and again what is here extreme capsule does the right and if you go to the top okay now what really happens from here this is of course what is the slope in the section right L and this is temporal lobe deep into this there the grey matter here right and here also what is this grey matter part yes please either the structure appear in many sections so you should have a very clear concept what is this grey matter deeply buried in sulla very good in sulla right so this is insula any question up to this and now I can make here your rag that is sitting what is this caudate nucleus which body is over this then we are repeating it here and from here yes tale of the caudate and here it is yes hadatha caudate and some of it grey matter is approaching through the most interior part of in capsule tada what is this lenta from nucleus same is on this side oh you are looking for put um and yes we have to ask this right where is the put a man because this red loves the put a man yes that's very important again I will go to put a man again now you will identify structures up to now what is this Halima right what is this internal capsule what are these structures together lengthy form nucleus this outermost part of the lengthy from nucleus this is called poutama you know right love to lick the Futterman you look here from anterior side so this is kutiman and more medial to that there is Globus Politis there's Globus plied us so we can say lenta form nucleus consists of put Amell laterally and Globus pallidus medially is that okay any problem up to this and now of course these are your beautiful what are these hello my and I want to make some structure here under the column I yes who will tell me what are these structures please tell me something under the thala my must be sub Carabas what are they sub helymus and of course you must be knowing that here should be what is what structure should be here please tell me midbrain right so there have to be midbrain here and if I draw a section of midbrain here right this is section of the midbrain and here is cerebral liquid Earth of course you know there are superior colliculi here superior película here the most important structure which I am interested to draw here is yes what is that what are these structures substantia and in substantia is posterior part is very dark colored and very dense very dense grey matter we call it substantial pars compacta right and anterior part of the substantia is less densely packed grey matter so this interior part is called just please very good substantia pass yes pass reticularis ratty Polaris and here it is substantial yes pass compacta right now these are some structures which I have drawn here another thing you know this red caudate nucleus it stain is going under the what is the structure under the cheese right and the end of this tail if I bring this red out its tail has special Bell here a mass of gray matter special mass of gray matter which should be under this structure here right and here also tail goes internet and there's are some mass special mass of gray matter here you can just imagine this is a rag bread for planning to have a bell with the cat but right now they are having on their tail so these bells are called this messes of gray matter are called yes please a metal are very good so this is Nandu light body or a Magdala Magdala this thing is the right drawn some gray matters here but I now want to tell you exactly which components are considered to be basal ganglia and which are not part of the basal ganglia right but remember whenever in this lecture I speak basal ganglia it should be considered basal nuclei right so now after you have understood all structures here let me go into some classification and grouping of different gray matters here now basal ganglia are basically classified or grouped in two ways there is traditional grouping of classification or component and there is clinical clinical grouping or classification of basal ganglia now when we talk about that prayer additional classification of basal ganglia it includes which structures I will just draw apparently now you have to tell me what I am drawing what is it yes what is this lengthy form nucleus this is put amend this is protoman this is no bus ply does globus pallidus is it right then yes more laterally there was a gray matter here what was this yes lost term very good and there was another piece of grey matter here you remember your friend what was this quad 8 right and then what was this yes Magda Lightbody now these structures are considered traditionally basal ganglia traditionally we think that quad 8 nucleus lenta form nucleus which consists of Futterman and Globus pallidus and with that maglite body and colostrum these are the structures which are considered traditionally basal ganglia is their right but now most of the neurologists are following clinical concept clinically what are the structures which are considered basal ganglia I will repeat it now of course plenty from nucleus is included put a man with Globus liders right here if we cut what was this structure quoi did you know it was going like this and like that right and with these structures functionally there are related these two nuclei what is this subtly my and what are these substantia so subtly my here right and then what is here substantial yes Niagara actually clinically these are the structures which are considered basal ganglia right quad eight with lengthy form nucleus and what are these subtly my and what are these structures substantia now why we have put these structures with this clinically because there are special connections between the LNT from nucleus and subtly mess and lenta from nucleus and substantia because functionally they make one unit and they're very important connections in between them so now the modern concept is that these structures should be considered basal ganglia and associated nuclei and colostrum and a magnetic body they will be now just they are studied separately especially mental and body is studied with the limbic system does their right which is concerned with emotions and memory and some other things is that right so clinically what are the basal ganglia lenta form nucleus corded nucleus and these two basic structure now another thing there are few more terms in which which should be very clear now now onward I will draw only left side of the structures right already you know this is put Amin and you know this is Globus pallidus global supply does is again divided into two part this is external part which is laterally and this is internal part which is yes medially is that right so global supply does as I can put it here that it has medial most part and lateral part right medial and lateral vien right this is Globus pallidus lateral or Globus pallidus external and this is Globus pallidus internal why I am stressing this because connections and functions of these two are different in a few minutes we'll see is that right now draw not the whole corded now onward it is just a section of its head here so this is your red head what is the head cord it is it right now come out of these structures which structure is called corpus striatum which structure is called corpus striatum because we have to get some terms now clear you think okay let me tell you all of them our corpus striatum before you tell me new things all of them are corpus striatum let's put it in this way for classification purpose that we put it here quad eight right what is this here lent it from nucleus as one component Budiman which is and here it is Globus blighters actually all these structures together are called yes all three structures or all three structures they are called corpus striatum corpus so try a dump right but there's more there's another term which is called just striatum or NeoStrata that terms include caudate with Futterman caudate right with kutiman these two structures together they are called new stray items near striatum is that right and this structure is called Globus pallidus of paleo striatum or Globus sliders now again corded with Putterman why they are grouped together as new striatum and now onward in the lecture when I say nice try Adam it means I'm collectively talking about quadrat and put Amin but if I mentioned corpus striatum then I'm including all three things is that right so why these are put together quadrant nucleus and put a man because they have similar connections there are similar type of neurotransmitters right structurally and functionally not only both of them are similar even and biologically they are derived in the similar way right even though kudamon structurally is well connected with global supply does but functionally it is it should be grouped with what is this what a so quadrate nucleus with the put oh man they are called new striatum so this is our what is this new striatum now as I told you in the beginning put them in with what is this Globus pallidus together in the sections it look like a lens right surrounded by internal and external capsule so both of them together are also called Lenti from nucleus so what are the components of Lenti from nucleus lenta from nucleus include yes put a man with Globus flight if lengthy form nucleus is that right now I will ask you if I say what are the components of lenta from nucleus yes put them in with Globus pallidus if I say what is new striatum that is core date with put them in and if I say what is corpus striatum that include quadrate Putterman and Globus pallidus or corpus striatum is quadrant with the lenta from nucleus am i clear do you have any question here there's no now onward will follow the clinical classification right that now onward in our discussion basal ganglia means mainly yes quadrant nucleus put them and with Lobos blighters and what else special connections with substantia and subthalamic nucleus any question here no after discussing all this thing now let's come to the how these structures function this is the real important part of the lecture the what are the important connections are basal ganglia and what are the neurotransmitters involved and how the basal ganglia function right that's what we are going to discuss now again I'm going to draw the structure of left cerebral hemisphere now onward let's suppose here is cerebral cortex this is cerebral cortex here is your friend yeah the piece of cheese you remember what is this put Amin this is Globus fly - yes this is put Amin this is Globus pallidus external Globus pallidus external or lateral NOPA spiders and turn Ahmad medial right aha yes here is a structure what is this some thalamus and here is the structures what is this substantia any question up to this any question up to this there is no question and of course here is what is the structure column I this is the midline right now before really I make this circuit right I will put this structure in structure as its these connections in a bigger perspective but why we need to learn it actually the basic rule is and central nervous system about the motor system of course this is midbrain and pons and medulla and if you go down what is this spinal cord right now how do you things go over basic rule is all of you know that these are the political spinal fibers which will come down and control the motor outflow let's suppose there are neurons here going to this muscle and their neurons here they are going to alpha another group of muscle now these are lower motor neurons right lower motor neurons come out to the spinal cord as well as they come out of the what is this brainstem brainstem is also lower motor neurons coming out for the muscles of head and neck lower motor neurons are the neurons having the cell bodies in spinal cord in stem and these fibers come out and do motor innervation at neuromuscular junctions with the muscles right is there clear now all of you are knowing that fiber which comes from here right of course they will cross into medulla here to opposite side and eventually supply here and these fibers from other side also come over here and cross and then supply what are these fibers cortical spinal is that right now if we work back the basic concept of most of the student is that quality of spinal fibers start from this motor cortex and they go down and control that lower motor neuron because corticospinal fibers are part of upper motor neurons so poor motor neurons are coming down and rolling the lower motor neuron and being the motor activity is that right now actually before this are there a corticospinal fiber as well as their quality go nuclear fiber particle nuclear fibers are these fibers right which are going to the what is this is a cultic o nuclear fibers are coming from the motor cortex and sensory cortex to the motor nuclei of the brainstem is the right functionally corticospinal fibers and cortical nuclear fiber the one and the same thing particle spinal fibers are coming to the to learn motor neuron which are cell bodies in the spinal cord and cortical nuclear fibers are those fibers we are coming from cerebral cortex to those motor neurons which are present in the brain stem of the cranial nerves clear now actually a promoter neurons fire lower motor neuron lower motor neuron fire the muscles and movement occur but actually the real idea of some movement and planning of the movement that is done at higher level and this information how to plan a movement and what are the motor plants they are actually stored in basal ganglia and cerebellum now listen very carefully that motor plants are basically stored in basal ganglia and cerebellum right for example if you want to make a movement I have to take cup of tea so look here suppose here is the cup of tea just imagined and if my hand is here I will take it here this is one movement and I will bring it to my left right take a sip and then put it there now this is not one movement multiple movements have been done so first the idea came is there right now to bring the cup of tea to my lips and then taking it back it is already programmed in my central nervous system is that right now those programs are we're in basal ganglia and cerebellum it means these upper motor neuron activity right this should be in close association with basal ganglia and cerebellum formation cerebellum will study sometimes else today we are talking about basil ganglia so what I want to stress that these fibers which are coming down right when idea of the movement start this idea should not go directly from here to here first it should consult the basal ganglia basal ganglia will plan the movement right initiate the movement and then eventually once cerebral cortex conserved the programs of the basal ganglia and then basal ganglia should give information back to the cerebral cortex then information should come down it means there should be some loop if this is supposed whether ganglia right this is whether ganglia something should happen that one movement planned start information should come here and then it should go yes through the thalamus it should go back and influence in the same way plan of the movement should come here and then it should go back so this is very important concept that basal ganglia have electrical activity even before you start the movement you just think of a movement if you just plan that you are going to do something basal ganglia start firing even before the movement really start am i clear so this is very important concept that idea of movement when you intend to do a movement right consolidation should be made with basal ganglia and then basal ganglia through the thalamus through the thalamus should fire back and then final orders are given to the cortical spinal and cortical nuclear fibers any question up to this right now let's see how cerebral cortex consult with the basal ganglia when it intends to initiate a movement right when it want to start up movement I will put lateral aspect of this also so it becomes more clear that what we are going to do and what is the importance of connections and functions of basal ganglia I'm making the lateral side of cerebral central our system right so this is preset this is central sulcus what is this pre central post central right and of course you know all those things now the important point which I want to tell you this is primary motor area is that right and what is this primary somatosensory area motor fibres which come down they come from primary motor area as well as from primary sensory area when Israel don't understand why they come from sensory area but actually corticospinal fibers and cortical nuclear fibers which come down they come from primary motor area as well as from primary somatosensory area plus they also come from pre motor area this is pre motor area and also comes from this structure and on the medial side supplementary motor area so what are the motor cortex motor cortex consists of pre motor area supplementary motor area primary motor area and it is functionally also associated with somatosensory primary area now what really happens when you think of a movement movement is originally idea of the movement come from the this area what is this area prefrontal cortex this is the cortex which thinks right for example if you are planning to throw a flying kiss to someone right so first you have to think you don't throw to everyone isn't it but sometimes you plan to throw it but you don't throw it with an idea one here but it was not executed but if you are really trying to going to do flying kiss for someone first you'll think the idea then things should go yes idea should go to the promoter area and supplemental motor area now look here basal ganglia the group right then what should happen this should consult basal ganglia right about the motor program but water program should go should it be a more romantic or less romantic gesture right then from here through the thalamus this information will go back here and from here then fibers will come down and then your hand will move so what I'm saying at one side is the idea of the movement in the beginning in the end there is muscle is that right there is pre motor car what does this idea start from the prefrontal cortex it will go to supplementary motor and premotor areas and these areas will consult basal ganglia and basal ganglia will refine the movement and gives special signals or feedback through the thalamus to the premotor supplementary motor as well as primary motor and somatosensory area from beam areas then fibers will go down as particles final or cortical nuclear any question up to this you are not confused yeah this is very important when these fibers come to the basal ganglia then they go to the thalamus and telev of cortical fibers go back to the motor areas premotor supplementary motor as well as primary motor even somatosensory area from all those area upper motor neurons come down am i clear so Kanna can we put now basal ganglia exactly where they are in our relationship of functional relationship the cortex has to consult the basal ganglia and through the thalamus information should go back and then upper motor neurons will file down any question now will come into detail how the basal ganglia work is there right I want to make a little more beautiful diagram now this is put Amin right but actually in this diagram I am showing only put a man but when I talk about put a man it should be considered in association with quadrate nucleus and you know caudate nucleus with the katana called new striatum what are they called neo striatum right and this is of course Gluba spiders right now let's start with the how the system start first of all when you are going to do movement context should yes connect with the basal ganglia so cortical fibers yes they come down and the stimulate neurons in neo striatum they stimulate the neuronal striatum this is striatum again I am repeating coordinate plus what is this put Amin for motor purpose most of the fibers go to the put Amin anyway so I will call it now onward striatum but not corpus striatum because when we say corpus striatum it include Globus - also I will just say striatum so these are political striatal fiber what are these called echo straight or fibers right then from here where important connections are going to the what is this Globus pallidus internus right and from there from there fibers are going what are this thalamus and then it should loop back and then it should loop back so what is this look here Fievel start and this this is a very simple note things are going directly back this is also called direct pathway right now what is direct pathway we'll talk in later in detail first of all what is this quantico striatal fiber then what are these fibers striatum pralaya del fiber to the internal locus pride is internal then play dota lemak fiber well I do telomere fiber then tell him of cortical fibers do you think it's difficult to understand so very simple now first of all I will tell you when you are resting and not doing any movement what is going on first we should understand when you are resting and not doing any movement what is going on in this circuit and then we'll discuss when movements start a plan of a movement you start right then what fighting occur first of all these red neurons are releasing stimulate pre neurotransmitter red neurons are releasing stimulatory neuro transmitter the neurotransmitter released by this is glutamate what is the late release from here gluta made and this is also releasing yes gluta made so fibers coming from the culture to basal ganglia of glutamine energy and from thalamus going back and also glutamine algid now when glutamine is release glutamate is released from this nerve ending to this dendrite or cell body glutamate receptor will produce K time influx when there will be a tiny influx this will get stimulated so glutamine urg'd fiber will stimulate this first neuron striatal neuron then striatal you wrong releases normally what GABA gamma-aminobutyric acid plus substance P this neuron when this neuron is stimulated its nerve endings release gamma minus Q Tarek acid along with the substance P and then Narada Lucas played as internist right so this neuron should be considered gabaergic neuron and the next neuron in the line which is concerned with the plight of hellenic pathway that is also Gaborik neuron what is that that is also gabaergic neuron and again glutaminergic now first of all I will tell you what happens when you are not doing the movement when you are not doing the movement these cortical spinal fibers which are going to come down you know this fiber which were coming down let's suppose I show that fiber here here I show cortical spinal fiber of course they are going down and lower motor neuron going out is their right to a muscle now when you are not doing any movement it means these neurons are not firing this is right it means motor cortex is over functioning or under functioning when you are not doing the movement you look throughout the lecture will use the logic when you are not doing the movement motor cortex here should be under functioning or over functioning under functioning it should be inhibited this is all right actually how it is kept inhibited when you are not doing the movement actually when you are not doing the movement when you are at rest Globus spiders in turn is actively firing when you are not doing the movement Globus pallidus internus is actively firing when global spiders internal is actively firing it is releasing gabon thalamus on which nuclei of salamis basically the nuclei of salamis is ventral interior nucleus ventral lateral nucleus central medial nucleus dorsal medial nucleus but anyway listen what I am going I am going to tell you that normally when you are at rest you are not doing any movement playdoh kilometres are very active right these five play-doh salami fiber the GABAergic fiber releasing fibers and these fibers are keeping releasing lot of gaba inventor anterior nucleus of Salamis went to lateral nucleus of Salamis and dorsal medial nucleus of calibers is that right now when gaba is released on these neurons gamma-aminobutyric acid is stimulator ii neurotransmitter or inhibitory it is inhibitory because when gaba is released on a neuron gaba receptor either allow the chloride influx and make the neurons very hyperpolarize or gaba receptor allow the potassium efflux and again loss of potassium Mazen you not very hyperpolarized so what happens Gamma minor butyric acid is normally released by Plato thalamic fibers right tonically and very high amount when you are resting and they keep the LMO striatal or sorry tell mo cortical fibers inhibited you are under straining when these neurons will be inhibited so naturally can they stimulate this no so movement will not be there you understand it this is what is happening at rest and you repeat it what happens at rest say rapidly there's a heavy firing by Plato Hellenic pathway which are GABAergic fibers releasing lot of gaba inventor interior ventral lateral and dorsal medial nucleus thalamus gaba inhibit these neurons then what happen thalamocortical fibers are inhibited no action potentials so these fibers do not stimulate the upper motor neurons pyramidal neurons going down to the lower motor neuron that's right now you are resting suddenly a nasty idea came to your mind and you decide to make a certain movement you're going to do a certain movement I will not tell what movement but certain movement now if you're going to that certain movement what will happen first of all you need to consult basal ganglia secondly this is automatic break of light of the basal ganglia basal ganglia is keeping an automatic break on the motor system that should be released so exactly what happened when you think of a movement right let's pose these neurons planar movement and they stimulate this now cortical striatal fiber will come now corticospinal fibers are releasing what thing here yes please glutamate glutamate will stimulate the striatum Playa del fiber now when these fibers are stimulated lessen glutamate receptor of the present here right glutamate will bind here gate ions will be loaded and this neuron will become active action potentials will move through and then release here gaba so this first blue neuron Australia to Playa del fibers release GABA implied earlier on when they will release govern the playa del neuron these ply the neurons go Globus pallidus internus neurons will be stimulated or inhibited here inhibited right so let's put it like this first of all these neurons are stimulated when you are planning to movement they are stimulated their activity is going up and when their activity is going up what they release here glutamate when they release the glutamate here what happens to activity of this neuron it goes up so these are also yes stimulated and when these neurons are stimulated striata why does internal neuron they release what substance here gaba and then they release GABA what happened to this neuron Plato Tel Aviv pathway there are two important pathway here one is and cilenti klaris other is lenticular fasciculus but anyway important thing is concept here when first inhibitory neuron in the habit the second blue neuron right now this will be inhibited so action potential in this neuron will be more or less less so what happened activity become less here an activity become less here then tell him of article fibers are released from the poloidal exhibition because when you are resting this these fibers were too much firing and kita kilometer off inhibited but now when we do decided to make a movement Carl Tico striatal fiber which are glutamine object stimulated the strai oh no buzz in terms of fibers when these fibers got stimulated they released inhibitory neurotransmitter on to idle neurons and hydrothermal fibers get inhibited and when they get inhibited then there is less gaba release attention please when these fibers get inhibited less gaba release in thalamus so telemeter ons are less inhibited or you can say they are disinhibited or this caveman is efficient is that right so when they skipped an efficient they start firing and message goes yes message goes to upper motor neurons and they are stimulated and fibers go down lower motor neuron the stimulated muscle contract any question up to this what is the role of thalamus here thalamus is acting as a relay station right that relay station number one number two very important thing Kalama says very intimate relationship even though it is at distance with the cerebellum there are lot of you can say fibers coming from cerebellum to eventually through multiple relate to the thalamus so thalamus knows the information in the cerebellum and information in cerebellum is what is the proprioceptive position in the body cerebellum knows which muscle is in which muscle or with joint or with tendon or which ligament is under what type of proprioceptive situation what is the degree of banded joints or what is the degree of tension at muscles or ligaments or tendons this information from cerebellum is being relate to helymus they are basal ganglia information and thalamic information they will be computed together and then final decision will go up that we'll talk later right let us come back any question up to this so so you need to understand when you are resting this this guru rather over firing lot of gaba in thalamic nuclei telomere nuclei inhibited telomere particle fibers inhibited no stimulation to the downgoing corticospinal cortical nuclear fibers but but when movement you're planning for a movement first of all quantico striatal fibers which are root of energy fiber stimulate the striatal neuron and striatal neurons when they get stimulated this pathway religious gaba in bloopers fly doesn't turn us knew Rosen Globus pallidus internus get inhibited then plied a thalamic pathway oh my god yes this get inhibited so glider Hellenic pathway does not release GABA in thalamic system and when inhibitory neuron is deficient here then thalamic neurons are released from the inhibition and the fire upward right to the cortex of course what is this this is going to premotor cortex supplementary motor cortex primary motor area and somatosensory area and there the neurons which are going down they are activated any question here this is called direct pathway right now we'll come to that fussy thing about indirect pathway what is indirect pathway let me tell you there is a lot more pathway when we start for the movement and let me tell you why we need to pass where's listen let's suppose my hand is like this okay my hand is like this and I want to close it right so move planing motor planning should be of two type number one flexor should contract number two extensors should relax are you understanding even when you are going to do any movement these posture your posture should be adjusted right and torn in other muscles where active movement is not done also need to be adjusted those are right for example right now if you are writing something try to write not only your hand muscles will change their movement but you'll find shoulder also has change in the MU in that tone try it try to write something it means actually basically this is a function of the basal ganglia we originally nevermind we planned to write something with the hand but why all this tone and postural platform is altered this is also all planning by the basal ganglia is that right now one thing which is important as I told you that if I have to close my hand flexors should contract but at the same time extensors should relax it means basal ganglia should have two pathways one pathway should be stimulatory to some muscle group another pathway should be inhibitory to other grow it means agonist should be stimulated and integral should be inhibited it means there should be one more pathway because this pathway is only stimulated now we'll talk about the second pathway look here this is when we are planning for the movement another pathway here it is initially it is the same what is it called the cost rate or fibers from the these are glutamine urg'd fibers and from here fibers go to Globus flight as externus not internist you see this is going all the way low bus riders in turn us the direct pathway but when we talk about indirect pathway the fibers from striatum go only to the glucose riders externus from there the next neuron they go to what is this sub columnist right and then from sub columnas glutamatergic neuron go to what is this flight up and from the fly damn glove was played as internals now neurons are going to Talam us now this pathway involve an extra loop here the fibers are going from striatum listen from striatum directly to Globus pallidus internal so this pathway was direct pathway here the fibers are going from striatum to external locus predecessor nam via the sub thalamus go to the Globus pallidus internal right so look striatum is influenced in the output of Globus pallidus internal directly or indirectly via Othello's so that is why this pathway is called direct pathway and this is called indirect circuit or indirect loop or indirect pathway am i clear so what is the indirect pathway where striatum is influencing the activity of Globus pallidus internal indirectly via a loop through subshells that's not right now how this pathway work again the cortical striate or fiber that glutaminergic and they will stimulate so again these fibers are what when you're planning the movement these are stimulated action potentials are more in these glutamine RG fibers but these glutamine are cheek fibers are different than the previous fibers because these fiber end up on such striatal neurons which go only up to Globus pallidus external right so they will stimulate first this blue neurons and when these blue neurons will be stimulated their activity will increase is their right but what they will release on the next neuron yes what they will release these neurons will release GABA when gaba will be released what will happen to the activity of this neuron it will be inhibited so we can say activity in this neuron is less when activity is less in this new wrong right which is no both gliders externus to subtly mas when it is less active it is releasing less gaba on these neurons right when it is releasing less gaba it means this is less than Hipple tree this is right so it means this will be released from inhibition and when these fibers which are subtly more idle fiber when these fibers are having less gaba influence they are having less inhibition or we say there disinhibited so they are their release from the inhibition so they over fire and then these fibers will over fire they will release Laura what is this glutamate in which area biloba spiders enter now and when there is glutamate released that was stimulate this pathway and when this is stimulated oh my god yes that's right these fibers will be stimulated so they will produce more gaba we're in thalamic nuclei and when there will be more gaba what will happen to this neuron this will be stimulated or inhibited that will be inhibited and this will be connected with some those system which need to be inhibited maybe in this example this pathway this pathway is bringing information eventually to the extender so extensions will be inhibited you are understanding no problem in this why you are looking so happy you are understanding it okay that's good I'm happy for you now again start the direct pathway and then we'll discuss the indirect pathway then we'll make their comparisons right direct pathways now you people will tell me Quantico striatal fibers right but real difference is from here that stray oh yes from striatum GABAergic fiber are directly connected to global spiders internus and from there fibers are connected to the thalamic nuclei what is happening when direct pathway is activated particles straight or fibers release glutamate stimulate the strai of Lydell fiber stimulated stri of light or fiber which are gaba rigid fibers with leaves of a substance P they release GABA internal cleitus group of spiders interest new neurons those neurons are inhibited and when they are inhibited they did they don't release GABA in the thalamus so Kelly will neurons are not anticipated so there will be over firing and when thalamic fibers which are thalamocortical fibers the over firing when they will go up they will stimulate the upper motor neurons is it right for one group of muscles maybe suppose here flexor player at the same time we need to inhibit some other neurons so we can say first of all indirect pathway indirect pathway when it is over firing quantico striae de what will happen it will stimulate the average neurons which are going from striatum to external fly down they will inhibit the fibers which are going from yes lado subthalamic and they're less relieved of gaba release in the subthalamic so sub thalamic neurons are not inhibited anymore the over fire and leaves glutamate in glucose fly doesn't turn on and glutamate stimulates an inhibitory fibers the Burchett fiber going to the thalamus and da release lot of gaba and inhibit these Telenet neurons and these telugu particle connections are inhibitory so what did we see direct pathway when it is stimulated it is stimulatory indirect pathways basically inhibitory does the right now let's compare and contrast direct and indirect first of all direct pathway is shorter pathway and does not involve sub thalamus indirect path is longer pathway involved the subthalamic connection direct pathway will stimulated eventually it stimulates the thalamocortical fibers so it is part of movement activation indirect pathway when it is activated it actually inhibits the thalamocortical some of that of course these will be different fiber those will be different it inhibit the Kellum of cortical fibers to inhibit certain upper motor neurons is that right any question here there is no problem now this is the basic connections now we come to role of dopamine substantial who is clear about this role yes you want to say something substantial Niagra what is the role of this actually these are the primary circuit it is like a fine tuner it's like modulator right the real action is here direct and indirect pathway this was now doing some modulation yes but help in the movement how look you must be knowing that there is substantial Niagra which is present in midbrain derivative of mesencephalon in whole this path wave it has the structure which are derivative of telencephalon eelain's fellows structures are to coordinate put Amin Globus sliders this is the right Dillons have blonde diencephalic structure is what is this sub thalamus and thalamus and measles belief structure is substantia right it is in the midbrain now let's see how the substantia work this is path this is path compacta this is path reticularis right now actually what happened yes from here Gabbar JIT okay I will not go into this connection but more important which is very very important phone action that from here what is this path from pattern right here are the neurons which are dopaminergic they release that dopamine what do they release their release dopamine and these dopaminergic neurons go up and release dopamine on both pathways now these are dopaminergic nerve endings it means that substantia dopaminergic fibers which can also be called nigrostriatal fiber influence the direct pathway as well as indirect pathway does that right then fluence the direct pathway as well as indirect pathway actually these dopaminergic fibers help in initiation of the movement they facilitate the movement now as I assume all of you are intelligent so you can tell me if this pathway supposed to enhance or initiate the movement kickstart the movement right this is the you can say kick starter off the motor system right and the motor cycles are the kick starter so movement initiator now this this neuron which are dopaminergic pathways it has to facilitate or initiate the movement you should be able to infer yourself that what should it do to direct pathway and indirect pathway if it should start the movement you know direct pathway is excitatory pathway and indirect pathway is inhibitory pathway if it has to facilitate the movement right so direct pathway should be stimulated or inhibited stimulated an indirect pathway should be inhibited so what really happens that nature has provided here d1 receptors when dopamine is released on d1 receptor right these neurons are stimulated and when dopamine is released same dopamine is released on indirect pathway d2 receptors d2 receptor produced inhibition of the neuron Paul am i clear what I'm talking about that is dopaminergic pathway and for instance that releases dopamine in striatum we call it nigrostriatal pathway right and some books it's written it stimulates some fiber than hits other fibers but some good books are now telling that dopamine delays and direct pathway stimulate the direct pathway and dopamine release on the indirect pathway inhibits the indirect pathway question of that how one neurotransmitter and one side is stimulating the other side is inhibiting now we know that actually here in these two places that is scepter for dopamine are different when d1 receptors are attaching and when dopamine binding with d1 receptor neurons are stimulated it means they're cationic loading cation will go in but when the permian will bind with d2 receptor in Trussell the signal signaling will eventually lead to K time release from the neuron neuron will be inhibited those all right now rest of the story should be very simple what should happen and dopaminergic system it's facilitating the movement and dopaminergic system is facilitating the movement what should we do it should stimulate direct pathway it means direct pathway stimulated this is a right what will happen more GABA coming here and internal is a neuronal level fly doesn't anima inhibited and there further the lesion more firing for direct movement right at the same time this is producing a very fine balance there are at the same time they are inhibiting the indirect pathway because d2 when this neuron is inhibited then less now here it is reverse not what is strong actually it will become less active what is this under the influence of dopamine right and less sector so it will release less gamma here so this path will be less inhibited so produce more gaba gaba will inhibited a lot and this activity will go down so it will not be stimulated it will be less active are you understanding and when it is less active less gaba over here this will be also released so basically dopaminergic firing on both side increases the action or you are looking a bit confused indirect pathway yeah let me tell you when we talk about called eco Strider system right this to belabor this pathway increases the movement and when quantico's try to pass become too indirect it decreases the movement right right but when we talk about dopamine right nice go straight or pathway this is the right what it has to do it as to facilitate the movement more for this purpose specially it stimulate the direct pathway I told you direct pathways excitatory pathway or movement initiatory pathway this is because concerned with the antagonist right this is inhibitory pathway so listen again final movement occur depend on what thing motor cortex activity depends on what same motor and cortex activity now motor cortex activity is normally increased by direct pathway normally decreased by indirect pathway is that right but if nitro striatal facilitates our desired movement desire movement is supposed to take close my hand so for this purpose it should enhance the activity in direct pathway and inhibit the activity and direct pathway am i clear are you clear or not how the court has talked to the listen yes I was thinking that one of you should be really intelligent that how that substantial Migron iran's know when to fire and which group of neurons to fire and reared yes of course they have very close the relationship what are these fibers cortical Negril fiber so this information substantia knows what is the planning going on and it will further fine-tune it is that right any question up to this yeah but it is less than a battery if let me tell you exactly tell you how what it happens basically when you plan a movement body are the tendency to overshoot in the movement so we have to find regulators will get this concept more clear when I talk about parkinsonism when this pathway is destroyed what happened okay let me tell you forget about this path well start another pathway here it should go through this actually I have put it on the same neuron that is what is disturbing now what is happening this dopamine yes you can explain why not come over here and stay no problem it's okay you're still in Lebanon fear that you made a mistake still you should be appreciated for coming over to the board look I will tell them what you are saying you are saying when dopamine will come over here it has d2 receptors so this get inhibited when it get inhibited right you will stand there so that they can see it when this will get inhibited right then it will release less cava and this will not be inhibited its activity will go up when its activity will go up right this will be inhibited but actually there should be another connection here ideally speaking this is their right so what happens when they'll be more GABA here this specific neuron will be inhibited when this neuron will be inhibited there's less stimulation to another GABA right and what happened that will become let's excite it because it was stimulatory so that will be less excited less excited mean less inhibition to the next and that will be positive result let me tell let me tell you we want positive now we have seen a direct pathway does the right and we have seen indirect pathway indirect pathway is defined as a pathway in which subtly boss is involved right now we know dopaminergic action on the direct pathway no problem now we dopaminergic action on indirect pathway the point which you have to understand that glutaminergic activity and dopaminergic activity are antagonists to each other on these neurons this is the right what has happening they are antagonists through each other the how exactly it happened I am going to draw this complex here suppose this is the neuron right here it is releasing glutamate is there right and let's suppose on the same neuron what is being released here dopamine right so here is dopamine two receptors do come in two receptors and here it is glutamate now what is happening this is loading the cations in and this is the removing the cation what will be the action that will be the net of them am i clear not necessarily zero maybe this is the release more and this is less a fine tuning fine tuning there's a concept of fine tuning because we don't want it over inhibition in this pathway is that right or over stimulation in this pathway so what happens that this is to MU late in their direct what does this indirect pathway this is inhibiting and both of them are putting a balance there now what happens if the more action potential coming from here and they're less action potential coming here net effect will be stimulation if the less action potential from here and more action potential from here net effect will be inhibition how it happens that now I think this is a very basic concept in the neuronal cell body then dendrite their potential membrane potential keep on fluctuating depending upon the balance of stimulatory inhibitory activity is the right and neuron will file or not it depends on what is the net potential in that for example threshold potential is let's suppose this is having resting membrane potential - 90 millivolt right threshold potential is suppose plus 20 is that right now what happened in this neuron resting amount of potential is fluctuating like this when this is firing cations are loaded it's this is resting on potential this is threshold minus 70 when cations are coming this potential is going upward and from this side but when this is firing this potential is going downward so depending upon what is the net effect frequency of action potentials will be determined yeah that's right rest amount of potential has to reach to the threshold only then it will fire but if the student potential goes above the threshold then frequency of action potential will be change more it is above the threshold more higher frequency of action potential the right we have gone away from the topic let's go back listen again rather than making a new pathway for simplicity purpose even though different pathways do exist for simplicity purpose I will say that neurons in the striatum neurons in the striatum are under the glutamatergic effect from the cortical straighter pathways and they're under dopaminergic effect from Negros prior to a pathway right again but neurons in the striatum which are going to enter the Globus pallidus internal they are having d1 receptors and neurons in the striatum which are going to the global spread a sec sternum they are having d2 receptors right is that left now when nigrostriatal fibres fire right they have stimulatory action on the direct pathway and in Hafsah movement right and they have inhibitory action on the indirect pathway and by that day inhibit the movement a mic left they inhibit or enhance no this is the question a here in house let's remove it because this is for that action let's start with D - now previous this guy this is shown GJ another actually depicting action of glutamate on this neuron now I am going to draw the arrows according to the action of dopamine right now you see dopaminergic action again I will repeat first direct and then indirect you people will tell me when dopamine leaves don't direct pathway what will happen to this neuron enter fight over fire over fire now you see it means this neuron over fires on blue time energy stimulation as well as over fires on dopaminergic stimulation so both of them go to quantico what is this particle straight you'll fiber the nigrostriatal fiber both of them stimulate the direct pathway then it is stimulated of course more gamma here then these fibers are inhibited and less Govinda what is this calamus and thalamocortical fibers are released from inhibition and more activation yeah here here they are antagonist because particles striatal fiber are stimulating the neuron now average neuron here but though Nigel's title fibers are inhibiting it so they're in Tekamah injection of each other now we see purely the action of negros title pathway when I blow striatal pathway is stimulated indirect pathway also receives more dopamine because it is G 2 receptors so what happened when d2 receptors they are yes more dopamine here he is neuron get inhibited the neurons get inhibited the next neuron are not inhibited at all so they will over fire am i clear when they will over fire they will release too much gaba here and inhibit his neurons and when they will inhibit the glutamatergic neuron from the sub Halima's going to the Lobos sliders less glutamate here less stimulation of the poloidal fibers and less stimulation means that activity will become less and less inhibition of thalamic nuclei right when there's less inhibition to this they will over file and what will happen that under the effect of dopamine direct pathways also stimulated and eventually indirect pathway also stimulate reaction in the end on the motor cortex yes please your question come over here or directly tell me where you are talking about come come yes your question is anywhere you put your finger and tell me your question your question is about the GABA when you increase basically when you're increasing gaba mm-hmm you're decreasing the firing on the subsequent neurons yes how it happens that is what you want to know yes understand I'm going to explain it how was it he was dragging me into little micro detail he is saying when one neuron releases gaba another how the other neuron is inhibited that is your question oh my god okay what is your question then when you reduce gaba right right now listen very good his question is this that if first neuron is relieving less gaba then I usually make a statement that the next neuron is release from the inhibitory action and it's over fire question is that why it over fire first of all listen these neurons generate a very promiscuous they have connections with multiple different neurons connected with inhibitory and stimulatory all those neurons this is one thing so usually one mechanism is the multiple mechanism one mechanism that this neuron may be under inhibitory neurotransmitters as well as stimulatory and when inhibitory is dominating right it is keeping it away from the rest a threshold but as soon as this become off then other influences which are stimulatory they will win over this is one mechanism another mechanism is let me tell you some of these neurons which have a tendency to autofire they have Slee a sodium leaky channels right they have sodium leaky channels so all the times on sodium is trickling in right but this not okay I should make it a different color because you should not confuse with guard suppose V that sodium leakage and okay Tanganyika channel all the time some cations are going in and this is the gaba which is for example this is GABA a receptor and when gob act on this receptor chloride go then now okay times are coming from there but chloride is going from there so what will happen that effect of K times which are coming in is neutralized by this this is a right and this is not allowed to fire a mic left second mechanism is gabab receptors they are associated with serpentine G inhibitory system when gaba bind with gamma b receptors they stimulate the G inhibitory neuron protein and that actually stimulate alpha inhibitory and beta gamma unit beta gamma unit basically stimulate potassium channels and potassium is normally more inside listen and gaba binds with gamma D receptors these receptors are coupled with G proteins and gene hibbett rewritten damaged unit bind with the potassium channel some special photo chef channels and the open because Hashem is more in the cell but I shall start going out so gaba has two mechanism to keep the noodles inhibited either while loading the neuron by with in ions caller ID or helping the cations to escape so neuron remain electronegative more and more electronegative when gamma is less either colloids are not loaded or potassium is not allowed to leak out and if potassium is not allowed to scout it start accumulating and take the rest in through threshold am i clear okay any more question no question okay let's come back so what we are talking about you understand these two things right now another thing you may be thinking what is this what is this thing path reticularis particular substantial Niagra actually ideally power the reticle errors should be considered Downworld displaced Globus pallidus internal because this particular and global slightest return them have the same connection so these days path ridiculous of substantial Niagra should be functionally considered more like local sliders internal then to be the to function like substantial a graph path compactor this thing should be clear it means that the disk should also have fibers as global spread doesn't turn them as fibers going to hell em us this also should have fibers going to the helymus this is the right it should also receive copper Jake fiber this is the right so as a virtue fibers are going to global spiders what is this internal in the same way gabber cheek fibers also come ok copper jet fiber also come to what is this Globus whatever this substantia compared this as these fibers are going there there are also fibers coming here and from here which fibers are going forward gabber jet from here also fibers should be covered is that right for going no need to go through this detail just remember that power reticularis is just a functional knee displaced downward cordially displaced piece of gray matter from the Globus pallidus internal is that right ok after having all this discussion now the last word about this thing Heather told you that direct pathway and indirect pathway are under the influence of what is the same dopamine and neither dopaminergic pathways stimulate the yes direct pathway inhibitor indirect pathway then there is also counter balances on them what is that counterbalance counter balances that within the within the striatum they are cholinergic neurons and these cholinergic neurons have influence here as well as here but they have opposite their their action is exactly opposite of dopamine you know biological system is trying to balance itself so dopamine had stimulated reaction on direct pathway so estill korean will have which action on the direct pathway inhibitory and as still Conan will have what action on indirect pathway stimulatory was a right if you cannot remember that most important but most important is you remember the action of dopamine right or direct and indirect pathway and then remember Estelle choline is opposite to that any question here done now I'm going to remove this diagram and rapidly make it and you are going to tell me where which neurotransmitter is being released if you satisfy me only then I will move ahead in the lecture then I will tell you the pathologies of these pathways first review the physiology rapidly yes I am drawing the structure then you have to tell me what is the structure cortex yes what is this nucleus lenta form Putterman Australia term in tournaments sternums substantial Niagra what is this here subtly mess here is your friend thalamus now you will tell me pathway these are coming from cortex these fibers are cortical striatum I will make two pathway cortical striatum one for direct other foreign direct their release what substance here glutamate then what is this what are these fibers going the Virgie core blue terminal did and again from here what fibers are going the eject and what are these fibers kalamu striatal what are these new terminology what is this pathway direct pathway is that right again tell me rapidly what happens and this pathway files what happened to this neuron over fire more gaba here what will happen to this neuron under fire less governed calamus thalamus triad is so Kalam of quality of puff is released and stimulation of motor cortex and motor activity enhanced is that right now I'm going to make indirect pathway yes any question up to this now you have to tell me rapidly these pathways are built of energy they stimulate this blue neuron first neuron then this is stimulated this will release more gaba in what is this area Globus pallidus sternness the neurons there are stimulated or inhibited and more kappa calm these are inhibited when they are inhibited they don't release GABA here and gamma is not released what will happen the slow over fire and that will lead to over stimulation of the budget fiber going from litem to thalamus more GABA here and these fibers will be inhibited so actually when direct and indirect both path pathways are firing then some of the tenem of quality of fibers are stimulated and other God inherited is the right it means when we are doing initiating the movement of planning the movement actually some of the motor cortex need to be stimulated another part need to be inhibited does that clear okay then what was here from here also GABAergic neurons do come here but there and to here but more important concept is what is this from pars compacta which fibers are going up yes here are d1 receptors in your indirect pathway there are d2 receptors so dopaminergic pathways I go straight to pathway stimulate the direct pathway and inhibit the indirect pathway does that laughs of course when it will stimulate the direct pathway then this pathway will become more stimulated so it facilitate the movement at the same time it will inhibit the indirect pathway and when it will inhibit the indirect pathway then indirect pathways inhibitory action will be less so more stimulation left any question up to this there now we come to the dysfunctions of these pathways actually when these circuits are disturbed motor movement become abnormal motor movement become abnormal in some kind of Lian's and some kind kind of Leon's motor movement become less we say there's a hypokinesia and in other kind of Leon's motor movement become more and we call them hyperkinesia so it means basal ganglia lien and some diseases can produce hypokinesia and in other diseases it can produce hyperkinesia of this kinase yes this can idea that that when you are resting but producing abnormal movements is that right I told you this is what for for the basal ganglia is to initiate the movement as well as program the movement right now let's see if there's a lien in direct pathway what will happen if there's an injury to direct pathway what will happen the classical example of that is when direct pathway is less stimulated when there's injury to direct pathway it is under functioning now and wonder what circumstances this can under function one of the classical example is parkinsonism right you know in patients with parkinsonism what happened to them this is very difficult for them to initiate the movement the movements are slow the movements are slow we say this hypokinesia and if movements are very less or not there we say akinesia patient for Parkinson's disease in sands disease they have three problems number one there hypokinesia hypokinesia means less movement but truly speaking the difficulties in initiating the movement it is difficult to initiate the movement and movement velocity and extent become less so say hypokinesia second problem there is the rigidity I will explain all these things third problem is tremors now hypokinesia why this is hypokinetic syndrome why it happens so listen now let's start what is the primary problem and the real problem in Parkinson's disease the real problem in Parkinson's disease is degeneration of the neurons in past comparative substantia and these neurons degenerate then release of dopamine then release of dopamine from Nigro striatal pathway is less for example 50 percent neuronal suppose 80 percent neurons here are degenerated so it means the release of dopamine in striatum is less now we will see if dopamine is less what will happen is that right what was happening normally first of all normally what happened when we have you up to initiate a movement called the cuffs title fibers file dopamine sorry glutamate released normally then these gravity fibers over fire this is a right more gaba come over and flied up playa del fiber that fly totally new fibers are inhibited normally and then what happens in normal person tell mo cortical fibers over fire and stimulate the motor cortex to start the movement now what is the normal function of DEET one it is stimulating this pathway that is what we know already now we see that dopaminergic activity here is less these neurons degenerated now if dopaminergic activity is less here then what will happen here is less stimulation more stimulation less stimulation it means that these neurons will activity will be less than normal it's all right again in Parkinson's disease where neurons degenerating paths compacta substantia what really happens the release of dopamine is less here when there's less stimulation of d1 receptors then these fibers we just try out plight of straight applied or fiber they are not as active as they should be to initiate the movement they're less active because they are no more stimulated by d1 receptors when they are less active they are releasing less dopamine they are leaving left to communion ply them and they're leaving less dopamine implied um then pride Allianz are less inhibited or their disinhibited a mic left so what will happen to these neurons they will slightly over fire when this is slightly over fire they're slightly more GABA and helymus and if there is more GABA and thalamus tell about quality of fibers are inhibited so this activity is less so thalamocortical neuronal activity is less then motor cortex is stimulated less if motor cortex is stimulated less due to less stimulate reaction of d1 receptors on direct pathway if this activity is less it is easy to initiate the movement or difficult to initiate the movement it is easy to start a movement or difficult to start a movement yes difficult to start the movement right any question about this system now second of course when in Parkinson's disease the nigrostriatal pathway not only provide less dopamine or direct pathway they also provide less dopamine on indirect path when indirect pathway is having less dopamine it means now d2 receptors are less stimulated and when d2 receptors are less stimulated what happens to these neurons they are less than habited because ritu receptors inhibit the neuron just specific neuron so what will happen that they're less inhibited so they will under fire or over fire yeah when they will over fire more gaba here and this neuron will under fire so less in gaba here and less inhibition to this and now subtly mo playa del fibers will yes over fire and that will lead to stronger stimulation of Lydell neurons and a slider neurons are strongly stimulated they release more gaba in thalamus and when more gamma is here now this neurons are also inhibited so what happened that direct pathway as well as indirect pathway when both pathways has lost dopaminergic activity both of them lead to less stimulation of motor cortex when motor cortex has less stimulation then what will happen it will become difficult to initiate the movement right and we say patient has hypokinesia akinesia this person if he has to walk he will walk slowly this poster will be Stube and he will be walking with very little steps is that right even if this person is standing you push him he start walking you initiate him a little rather than Nigro straight or pathways you push him so he start but it was difficult for him to stop now because for stopping you need different kind of movement initiate the opposite result you are understanding so in Parkinson's disease they find it so difficult to initiate the movement that their face look like masked face because the don't show expression normally when someone is interacting with you your facial expression keep on changing to change the facial expression muscles of facial expression should work and motor cortex should work you know when to smile and when to frown and when to do blink is that right but a person who is having this problem parkinsonism nigrostriatal can he initiate the movement even to smile or to frown or to blink they find it difficult is sometimes they don't blink for very long time we call that as if they are having serpentine look with mask face as if they are having a mask on the face without any expressions you are understanding now then rigidity actually when you tec check that tone right tone as a cost of muscles what happens motor cortex motor cortex is having some action on their part core reticular fibers and from the radical formation fibers go to spinal part which control the tone so cortical reticular and reticulospinal fibers is there right they control that tone now what happened when cortex is inhibited then quantico reticular fibers are working less when cortical reticular fibers are working last reticular formation / v right let me draw a diagram this is a cortical reticular fiber and these are ridiculous spinal fibers and they determine that tone is there right now what happens and cortical activity is less then cortical reticular fibers activity is less is the right normally quality core radical of fibers inhibit the reticular formation when these fibers are working less then they overwork and the over fire and the tone now when muscle tone will increase and flexors and extensors both right muscles on flexors and extensors both sides are more strongly contracted at rest so tone is increasing on flexors and extensors both so what happen when you try to flex his arm it is very difficult and we didn't you try to extend it is also very difficult you feel as if you are moving as if limp is like a rigid lead pipe you know lead pipe when you are bending the lead pipe all the range of the movement you have difficulty so this type of rigidity is called what kind of rigidity lead pipe rigidity is that right lead piping or lead pipe rigidity there another thing which is there is a tension I told you previously that here there are cholinergic fibers and call Inderjit fiber that opposite action on these two as compared Obama now you have to see here that dopaminergic action and call energy reactions are opposite to each other right we can say for normal function for normal motor function there should be balance in dopaminergic activity and cholinergic activity in the striatum just that clear now what happened but dopaminergic activity go down the relative activity of cholinergic become more is that right am i clear or not when Parkinson's disease when these neurons are damaged dopaminergic activity become less then cholinergic activity become unchecked because normally dopaminergic activities is exactly opposite to call energy activity dopamine was inhibiting the sorry stimulating the direct pathway and inhibiting the indirect pathway estelle choline is inhibiting the direct pathway and stimulating the indirect now when dopaminergic activity become more another thing happens there are a lot of motor programs here and there are some circuits which are called reverberating circuit reverberating circuit mean that neuron is going forward some fibers come back and reach stimulate the previous neuron so action potentials move in a circle are you understanding me yet within this system there are some neurons which are making a reverberating circuits circuit mean fibers like the section to the moving like this when dopamine is less and acetylcholine is unchecked these reefs perforating circuit become fast and they become fast what happened even during the resting conditions agonist and antagonist people working in alternate fashion flexural flexors extensors keep on working in alternate movement what will that produce primers and what are these tremors the resting tremor your understanding so imbalance of dopamine and a spell choline producing kill role in resting tremor right stooped posture mask face difficulty to initiate the movement and if you really walk with shuffling gait any question up to this pardon why we have these reverberating systems here actually what happens sometimes they act as an amplifier let me tell you how reverberating pathway this is a neuron we stimulate the next neuron that stimulate the next neuron right now what happened from here one connection come and stimulated from here another connection come and stimulated so you gave one stimulus here when it one stimulate went had it bifurcated here an automatically second pathway vent head from here a third stimulus went head so in this way you can sustain certain flow of action potential you are understanding it so these are present over here to maintain specific tone and flexors and extensors when reverberating circuits are disturbed right listen now if I'm keeping my hand like this resting position there's a specific tone degree of contractional flexor and extensor and I'm making it steady is that right now the free perpetrating circuits are disturbed sometimes they will over flex then they will try to correct it and overextend then they will again try to correct it on over flex so in this effort they will produce resting tremors am i clear no problem right okay this is what happens in Parkinson's disease in Parkinson's disease there are different type of parkinsonism one Parkinson's disease with me and I grow straight all pathways degenerated then another condition which was called MP TP associated parkinsonism actually this was a situation which was discovered in California that some young people were getting Parkinson's like features so doctors are very upset you need this is an old age disease then they came to know most of them were actually heroin addict and they were taking street heroine the heroine which was provided to those people was of low quality I mean there was some contaminant in that and that contaminant was with - I'll Tara Pyrrha Dean anyway this was substance which was contaminating that heroine or addiction material and when they were taking this material they came to know this compound MPTP could damage the nigrostriatal neurons and what was happening patients were developing in very young age Parkinson's disease like situation so this were called and PTP associated Parkinson's disease then Parkinson's like situation can also occur if you are giving a patient dopamine receptor blockers if some patient is given dopamine receptor blocker the drugs are antipsychotic drugs if those drugs are given and these receptor the block functionally it is like losing the nigrostriatal pathway times when you when you give the patient anti-psychotic drug they may come after two weeks back and now they say okay of our psychosis is okay or not but we have developed new problem we have this shaky palsy and we cannot move around you understand it so that is drug-induced parkinsonism anyway this was a few words about parkinsonism so this was a classical example where in the deficiency of dopamine lead to reduced stimulation of direct pathway and reduced stimulation of direct pathway eventually reduces the action in motor cortex and hypokinesia any question here now I will talk about diseases disorders of basal ganglia which produce hyper kinase they are of dyskinesia remember these are only aliens don't produce paralysis either they reduce the movement or they increase or produce abnormal movement now you have understood how the hypo kind is di can occur now I will try to explain you that if there is some damage to especially indirect pathway look if direct pathway does not work you know hypokinesia now I will explain if this damage will direct pathway you may develop excessive and abnormal movement that is hyperkinesia or dyskinesia let me explain how it happens I think by now you must be able to teach it to some of your friends am I right or wrong [Music] yes this is your pathway you just tell me what path they have drawn direct or indirect right now yes it is direct pathway aliens of direct pathway produce hypokinesia but now I'm going to split limbs off indirect pathway to draw the indirect pathway yes this is your indirect pathway right and as you know that here it was in both pathways were influenced by dopamine right we have already discussed previously if dopaminergic activity is less here it will produce hypokinesia but now we will talk about something else let's post problem is with indirect pathway let us post that due to some disease these neurons are degenerated or damaged if these neurons are damaged can indirect pathway work can indirect pathway work no now what happens if due to any reason these neurons regenerate which neurons gabaergic neuron which are participating in indirect pathway is the right but direct pathway is intact remember these two neurons are slightly different these were gabaergic neuron with substance P these were the Burchett neuron with an Calphalon so some diseases preferentially damage these neurons and other diseases preferentially damage other neurons so let's suppose there is a disease let me tell you the name of the disease kingdoms disease have you heard of it right in Huntington's disease on chromosome number I will go into detail of Huntington's later just for a while you trust me what happens these copper Jade neurons degenerate if these garbage neurons degenerate now you will tell me action on these neurons will be less or more less of course if 90% are degenerated GABA in this area will be less so when action of these neurons will be less GABA will be less so these neurons will be kept inhibited or not so they will overwork or under birth when later subthalamic fibers will over right when Gabbar chief neurons in the striatum part is putting an indirect pathway degenerative dysfunction then gabaergic neuron from Globus pallidus to subtly massage release from inhibition the overworked and too much gaba is here and when too much gaba is here that will inhibit these neurons so there is less stimulation - what is this will idle neurons are you understanding me when playa del neurons are less stimulated the less glutamate here they are less stimulated so they will fire more or less again I know you are tired again these neurons are degenerated right now they are overworking there's too much GABA release in sub telomers sub thalamic neurons are inhibited so sub thalamic neurons release less glutamate in Globus pallidus internal so Globus pallidus internal neurons are less stimulated by glutamate so because a less stimulated so there will be less active this is the right when they are less active lesson here when they are less active so gaba released in thalamus is less and tell him is neurons and total amount of gaba in the thalamus become less inhibitory Infernus on the thalamus is less so when true interior nucleus and ventral lateral nucleus will over fire and when they are over firing all that time they're over stimulated many neurons here going down and that will be producing excessive unwanted movements that's right and we say they're hyper kind as they are dyskinesia so this was in Parkinson is not a classical example of genesis of genesis of hypokinesia x' and this father genesis off yes hyper or dis kinase here's more movement or excessive movement or abnormal movement does the right any question in these two comparisons anyone who is not clear if you are not clear now I will commit suicide is it really clear ok now let's see what kind of hyperkinesia what kind of hyper candy ideas can be there ok there are different types of hyperkinesia we can say there Korea's there is a three ptosis there are dystonias and there are Bella's mas or hemiballismus all of them are excessive movement and there are tardive dyskinesia as I will explain all of them don't worry I think it was you were a born alpha explained our div this kind neighs yes ok there are other also but let me explain these first ok Wilson's disease Korea has Huntington's chorea tang tons Korea Korea also can be part of st. Vitus dance st. Vitus dance or st. Vitus dance is also called Sydenham chorea Sydenham chorea and there's another disease called Wilson disease I will explain them one by one in all of these diseases the dominant leonis in indirect pathway so in all of these diseases movement will be less or more yes there will be excessive abnormal movement now first of all Korea what is Korea yes it's North Korea or South Korea yes what is Korea I have you seen Michael Jackson dance Michael Jackson dance somewhat like Korea sudden brisk purposeless flying movements of the limbs uncontrollable what is this Korea is basically damage to this system right and when the GABAergic neurons in the what is this corded nucleus are damaged specially not in phenomena and GABAergic neurons in quadrate nucleus are damaged striatum right what really happens indirect pathways dysfunctional right and many motor programs are abnormally released I will tell you exactly how the Korea is produced many motor programs are abnormally released what I told you that when this Fox is inhibited then actually okay sorry it should be here when this pathway is not working eventually what will happen motor cortex will be under stimulated or over stimulated over stimulated now if motor cortex is over stimulated or from this area or stimulatory signals are going now in your central nervous systems you have different program for example this is a program to raise your hand right and salute someone this is the program to bye-bye there's another program you can run for example right there's another program now these are different programs which are there and you only use them in specific situation now if indirect pathway is disturbed and motor cortex is over stimulated it may release multiple program in in a haphazard fashion for example you are going to salute but half of the movement go suddenly it goes like this and then suddenly another program is leaking like leaking leaking of the program right inappropriate release of the program for scratching here but you come here and then suddenly goes like this what happens in Korea from central nervous system motor programs which are stored there are haphazardly released their components are released and they result into sudden uncontrollable or involuntary purposeless movement you understand Korea so it's just like a Michael Jackson latest dance this is it right now how Korea can occur one Korea Huntington's chorea you will study in detail in pathology but I will just tell you in Huntington's chorea what happened their problem is it is inherited disorders and Huntington's chorea chromosome number four on chromosome number four there is a special gene which is called Huntington gene in this gene prime nucleotide to repeat can they are amplified trinucleotide repeat are amplified and when trying in fluid repeats are too much amplified that produces an abnormal protein which is toxic that toxic protein damages the governor as well as cholinergic neurons this is their right so what will be the result basal ganglia dysfunction and that will result into Cori for movement with that these patients are also developed depression and dementia is that right and in Korea disease all the features of trinucleotide repeat diseases are there for example trinucleotide repeat diseases get progressively worse generation after generation so on typical Korea also get worst generation after generation father has less Korea and son will have or less real disease son will have more severe disease grandson will have very severe disease secondly because after every generation trinucleotide repeat amplifier disease get worse why is that I a nucleotide repeat amplifier because Buehring oh genesis of spermatogenesis trinucleotide repeats are over copied so children have more repeat than the parents you understand me now so generation after generation Huntington's disease get more severe and appear at younger age is that right what happens in Huntington's disease that specially head of the caudate nucleus degenerate and lateral ventricle looks as if it is abnormally widened because had head of the caudate nucleus is no more occupying its normal and anatomical position am i clear or should I draw a diagram it's really clear she just want to leave the lecture now I understand okay so Huntington's chorea is inherited disorder autosomal dominant related with trinucleotide repeat amplification disease get worst generation after generation and where disease appears at younger age generation after generation is the right the cause prior nucleotide repeat over amplify during gametogenesis does their right and try a nucleotide repeat which amplifies they consist of cytosine what is this adenine and guanine but you can remember caudate nucleus having less hostile choline and having less gaba quadrate nucleus having less Astral choline and less gaba core energy can cover chick new honda damn i patient as classically of a normal motor moko reform movement with that there is what else is there with Korra for movement depression and dementia is that right then there is sweet white of dance or other name is said enhance core here this type of problem is more common in girls and this is seen this is another type of Korea purposely a sudden breast uncontrollable movement if you really want to have Coria try to get this one not the other one Huntington's if it once started his progressive Saint Vitus dance or straighten hands Korea is transient Korea it occurs in the patient with rheumatic fever some people especially in younger age when they get streptococcal infection with beta hemolytic organism right some of these children develop cross immunological reaction and that mineralogical the immune system which is supposed to and streptococcal infection produce sore throat immune system should specifically fire back against the streptococci but unfortunately immune system also produce some component which react with our own tissues it means immune system cross-react we are supposed to fire against the bacteria but also fire against our own tissue and if this immune reaction injure the core date and produces inflammation in caudate then patient may get Korea but you will need is short term Korea right when it does the rheumatic fever become okay Korea will be terminated am i clear then there is another disease in which Korea can occur that is called Wilson disease and will send of these what happens that this is a this is inherited disorder of copper metabolism that there is a protein called ceruloplasmin ceruloplasmin level is less in the blood and copper accumulate into liver and copper accumulate in the cornea and copper accumulate into caudate nucleus and lenta from nucleus right so it damages the liver and damages the lenticular nucleus so we call it Hospital lenticular disease what we call it a pet or lenticular disease or Wilson disease it is copper overloading disease right in which when the black and the liver copper is more in the blood ceruloplasmin is less and urine looses lot of copper there's excessive expression of copper and uranium now in these patients when copper damages the liver patient develops cirrhosis or liver failure eventually when copper damages the basal ganglia patient developed Co reform movements or dystonias and when copper deposits into cornea in the cornea there's a Decimus membrane you must have studied in Anatomy you don't know this cornea the cornea cornea has one of the layer which is called Decimus membrane copper love to deposit there and copper deposits into Decimus membrane it makes a special ring in the cornea that is called case sir flashed in the ring right I don't know the Spelling's you can write it like this okay sir flashing arraigned right so case for flash the ring is deposition of copper in the cornea in which disease wilson's disease this is a pattern lenticular disease is there right cirrhosis can occur in the liver and it can damage that basal ganglia and produce abnormal motor movement claire de ja it is damaged it is progressive damage and it is a religion with chromosome number 13 right this genetic inherited disorder if you really if you are really desperate to get Korea try to get certain hams Korea right that occurs in children do really between 4 to 14 G or 15 gr or up to 20 here all of you are above that a rheumatic fever may have Korea's a part of it right that is Sydenham chorea or sometimes females when they get pregnant in second prime minister they get to the certain hams Korea that is also called Korea gravidarum that curry of the pregnancy but it's rare don't worry okay you want to know rheumatic fever okay so very briefly I will tell you dramatic fever what happened special type of streptococci beta hemolytic as Lancefield group a prometo genic strain these special strain attack the strep throat most of the people when they get this infection most of the children they make antibodies which only damage the bacteria we are happy but in 3 percent of the children unfortunately when these bacteria attack the throat immune system fire back against the bacteria but also attacked some of our own tissue which have some antigens which are like bacterial antigens that means the immune system is really stupid rather than making very specific antibodies against the bacteria it also makes antibodies which also cross-react with our own tissue so those antibodies may cross react with our cardiac tissue or with the synovial membrane so patient may have called itis myocarditis pericarditis or endocarditis or polyarthritis and skill liens or the he may have Korea or some nodules in subcutaneous tissues you will study this in pathology one day hopefully right anyway so aren't interns can produce Korea which is due to degeneration of GABAergic and cholinergic neurons right Wilson's disease can produce Korea copper deposition there st. vitus Korea when immune system attacked the basal ganglia but it is transient well notice III ptosis Korea you know it is Michael Jackson dance what is H V ptosis have you seen Indian dance Indian classical dance cut sock dancer have you seen Indian dances or not okay if you really have some time to see Indian dances they are not haphazard movement like Michael Jackson they are different usually they move the hands in a very artistic way slow reading movements right so these are Indian dances what is happening the movements are in the hands of distal part of the limb and they're slow and finest no jerk is involved as if one movement melt into other movement and other movement melt into third movement third movement melt into fifth movement you get it very artistic movement sometimes patient does not want to dance but these movements are automatically released from basal ganglia and person is having slow sinus rhythm movements of that right these movements are called what acidosis right again this is a damaging indirect pathway and excessive stimulation isn't right all those diseases which can produce Korea they can also produce a theta says for example lesson now it's very easy to understand if motor programs are haphazardly and rapidly released that will produce Korea if motor programs are released very smoothly but automatically without any will and one movement convert into other movement smoothly this is a chi ptosis so many patients have korean method to assess both we say we should have choreo at she ptosis is that right so you have Michael Jackson dance here and here you have Indian classical dance now we come to the dystonias dystonia are when the muscles especially the muscle muscles are uncle muscles they are over contracting in a very prolonged fashion like this and it remains like this this is called dystonia and if in some dystonia neck is bent like this and very painful right we call it torticollis have you heard of it so dystonia here what is happening which movements are over released which movements are over released for uncle muscles and ziyal muscles is that right again when sudden jerky movements uncontrollable of the limbs what is that purposeless movement yes Korea and this will part of the limbs moving in a slow sinus movement acidosis and if these muscles are very long time like this and then like this what is this dystonias and then there is hemiballismus this is very dramatic have you seen arabic dance yeah you are not really - people right okay anyway you know Michael Jared NASA's what Korea Indian classical dances mitosis now if you see really classical Arabic dance you have seen what is the special feature of that it's very different from Indian dance yes they're violent hip movement and shoulder my dad and really don't want to show it so I don't know how to do it but something is happening very drastic to the woman who's dancing right we call it belly dance type or something right you understand it you know belly dance yeah every man knows it okay now actually if you release imagine a woman who's a rabid dancer and unfortunately she has some problem in basal ganglia should have very dangerous dance very provocative right now what really happens that that kite of dance can be called ballast masoor if this is half of the body hemiballismus let me tell you how it comes actually they're they're damaged in the sub thalamus there's damn I to subtly mess this is classically seen in patients with hypertension of the diabetic patient that when they were sleeping maybe the artery which was supplying to sub telomers that underwent from both Caesar hemorrhage and there's a small infarction of sub telomers very little unfortunate but in the morning patient will find that he is having a very dramatic it is one of the most dramatic presentation and clinical medicine you know what will happen when this is listen when this is what is this in fact I'd remember there are two sub tell ever saw one sub thalamus there are two now if this is suppose left sub Halima's these fibers will be controlling the left cerebral hemisphere from their particle spinal fibers come and cross to the right side so damages to the left left sub Halima's the clinical features will appear on the contralateral side or if clinical features on one side subtly muscles DeMint on the contralateral side now the sub column has specially controlled the hip girdle and shoulder a shoulder girdle is there right now if this is damaged indirect pathway is gone and there's a excessive movement especially about the hip or shoulder girdle now you imagine if person is having a sudden movement of this shoulder what will happen this ear will go like in a ballistic fashion like this this arm will go suddenly like this right or hip will certainly move and leg will be going to I don't know where is it right so usually it happened to one sub thalamus so half of the body is having violent jerky movement of the limbs initiated from abnormal movement of shoulder girdle or hippo garden you are understanding if it is unilateral we call it hemiballismus if it is bilateral unfortunate you call it Bell ism am i clear any problem up to this all of these are dis kinase yes all of them are produced due to abnormal function in direct pathway indirect pathway indirect pathway again certain Michael Jackson dance what is that Korea Indian dances what a Cheeto says Korea is certain purposeless movement uncontrollable movement of the arm right these are finest slow movement dystonias al muscles a tranquil muffled in high tone Hannibal isthmus one limp or other limb is flying in the air right due to certain movement in the shoulder of the hip girdle right so what is this it's like a rebel dance very violent movement of a / shoulder region right you can understand why shoulder region now last thing which is leftist tardive dyskinesia tardive dyskinesia is a disease which occurs in those patients who are taking dopamine receptor blocker normally we give dopamine receptor blocker to those patients who have psychosis you know what is psychosis schizophrenia type thin psychosis is the am sphere mental disorder in which you have lost the contact with reality is the right since psychotic patient one of the way to treat them is giving an dopamine receptor blocker now what happened attention please if you are giving a patient dopamine receptor blocker for a very long time if you're blocking these receptor for a long time but it will happen to receptors they will down the kool-aid or upregulate you are pregnant if you are blocking the receptor then cell will produce more receptors if you are or stimulating the receptor then cell will produce less receptors wow this is a very basic concept look this is a cell this is a nucleus this is the gene which produces a specific receptor right now if this receptors are totally blocked no action of the receptor is produced genes assume as if there are no receptors so they will produce more receptors you are understanding so what happens this is a regulation of receptor so what happens those patient who are given antipsychotic drugs which specially block the dopamine receptors right sometimes for wrong use of side drugs you'll need to up regulation of dopamine receptor then striatum we say that you should become hypersensitive to dopamine and this regulation will become disturbed now you see if there are too much receptors of dopamine here on indirect pathway then it will be excessively inhibited will it be inhibited or not excessively dopamine through d2 receptors and hibbett the indirect pathway you are understanding so it is just like damage in the indirect pathway and again what will happen this kinase will produce usually this type of problem occur in older people usually in females for 50 60 70 year-old and they have been given anti-psychotic drug for a long time and they dwell a very strange type of Korea through otic movement or abnormal movement you know what are these these are usually in their lips and tongue and in this area probably the basal ganglia which control this area there there's a lot of abnormality and these unfortunate old females previously they had a trouble they were psychotic and now they develop a new trouble after using the drug for a long time will they have abnormal movement of Jah lips tongue and all the time what they are doing they are like a fly catching movement of the tongue or smacking the left and they cannot control it they cannot control it right I am NOT will do it again right so what happens that this type of movements will do all abnormal orofacial movement uncontrollable movement lip smacking their own lips lip smacking our tongue flying movement and silt tongues not flying it's like catching movement as you've seen frog catch them or something right all these movements uncontrolled coming this is called tardive dyskinesia is that right so we have finished a lecture but before finishing it I will make a rapid review just in five minutes first of all clinically basal ganglia include yes caudate nucleus then butterman Globus fly does put a mana and associated nuclei are sub thalamic and substantia now quadrate with butterman are called neo striatum and put a man with Globus pallidus is called lenta from nucleus and all of them are called corpus striatum is that right number one number two direct pathway yes you know you were tell me from cortex what is coming down blue thumb energy fiber from striatum going to the plight of the aubergine fiber from Playa del to helymus which fibers the budget fiber from there back to the context what are this glutaminergic so what happened glutaminergic gabbar singh gabbar g glutamine urge if that's a direct pathway indirect pathway what happens no terminated fiber to striatum to the external global spiders which fiber the budget from their two sub Salamis gabber jig from sub helymus to play dumb internal below demeanor jig from there to tell Emma's GABAergic and from there to final up yes glutaminergic now direct path Fillion will produce hypokinesia or dyskinesias hypokinesia x' indirect pathways leaves will produce hi Bergen is er disguises yes is the right classical example of hypokinesia producing problem is Parkinson's disease where is the lien nigrostriatal pathway substantia right with the deficiency of dopamine dopamine Negros rate will pass code dopamine stimulate the direct pathway and inhibit de and direct pathway I still : inhibit the direct pathway and stimulator and direct pathway is that right now if direct path now what are the common King indirect pathway direct pathway short pathway direct pathway does not involve subtly most direct pathways Milgram energy grabber jig aubergine glutamine urgent direct pathway the secretory pathway Lien's of direct pathway produce hypokinesia x' and dopamine stimulate direct pathway clear indirect pathway indirect pathways glutaminergic GABAergic again Gaborik to sub salamis glutaminergic back to ply dumb GABAergic to calamus and then glutaminergic back to cortex this is indirect pathway indirect pathways longer pathway indirect pathway involves a subtly bus right sorry direct pathway stimulate the movement indirect pathway inhibit the movement is that right and indirect pathway aliens produce hyperkinetic movement or dyskinetic movement classical examples are Korea's like a Korea which can like which dance Michael Jackson dances Korea it occurs in which conditions and take those disease st. vitus which is in rheumatic fever and Wilson's disease in copper overloading disease right then we come to a Cheeto says it is like slow Indian dance that can occur also in the same diseases which can produce Korea then we have come to dystonias this is a hyper tone in the axial muscles or canonical muscles then we come to the list MERS where is the lien hemiballismus contralateral sub therapist this is like a rapid dance violent hip or girdle movement with flying limbs this is not right and then tardive dyskinesia these are abnormal orofacial movement Korea it rhotic orofacial movement produced in patient due to chronic use of such antipsychotic which are dopamine receptor blocker we are dopamine receptors become overexpressed any question here there's no question class dismiss

Channel: Dr. Najeeb Lectures

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Keywords: dr najeeb, dr najeeb lectures, basal, ganglia, neuroscience dr najeeb, neuroanatomy dr najeeb, neurophysiology, basal ganglia, basal ganglia function, basal ganglia stroke, basal ganglia anatomy, function of basal ganglia, basal ganglia pathway, basal ganglia disorders, what is basal ganglia, basal ganglia blood supply, basal ganglia direct and indirect pathways, anatomy of basal ganglia, basal ganglia physiology, basal ganglia connections, usmle step 1

Id: XE05j-O4sAc

Length: 147min 34sec (8854 seconds)

Published: Thu Mar 21 2019