Understanding Basal Ganglia and Pathways

welcome to section six in Neurology in this section we will be discussing the basal ganglia and the dopaminergic pathways so let's get started so the basal ganglia is responsible for smooth voluntary movements it's composed of the striatum which is composed of the caudate and putamen and the lenta form which is composed of the per Taemin and Globus pallidus it also has the substantia pars compacta and a c4 compacta and also has the subthalamic nucleus or stn for short now the basal ganglia contains the direct pathway which increases movement as well as the indirect pathway which decreases movement so now let's show some anatomy of these locations here is a sagittal view of the brain this is actually figure 8.4 which was discussed in section 1 of this chapter what I would like to have you focus on now is the basal ganglia as you can see the caudate is here it actually extends back and then it curves forward again and then we have the per Taemin which as this line indicates is right here and just medial to that is the thalamus as you can see here now the Globus pallidus is actually medial to the Petain 'men and you can't really visualize it here but if we were to take a coronal section of the brain and cut it through this portion we would see figure eight point five figure eight point five was also discussed in section one of this chapter so now we can see that the caudate nucleus is located here and that the thalamus is located here and then of course we have the / Taemin right in this region and the Globus pallidus external and then the Globus pallidus internus now let's show a slightly more posterior coronal cut of the brain on a new slide since we are more posterior than in figure eight point five shown in the previous slide we can see the brainstem right here and the substantia in the midbrain as we will discuss later in this lecture the substantia plays an important in the basal ganglia as discussed in section 3 of this chapter the red nucleus is also in the midbrain right here and right here and is the red nucleus and we will discuss the relevance of knowing that the substantia and the red nucleus are located in the midbrain once we get later in this lecture and discuss the dopaminergic pathways so now that we have our landmarks let's discuss the direct and indirect pathways of the basal ganglia so on the Left we have demonstrated the direct pathway and on the right we've demonstrated the indirect pathway it's important to recognize that both the indirect and direct pathways are on both sides of the brain but for simplicity in this lecture we will illustrate the indirect and direct pathways separately on separate parts of the brain so now let's first discuss the direct pathway so the direct pathway is the excitatory pathway which means it increases movement and the pathway starts in the motor cortex which then stimulates the striatum specifically the caudate and the putamen at which point the neurotransmitter gaba is released and then we'll see inhibition of the Globus pallidus internus which causes decreased inhibition of the thalamus specifically acting on the ventral lateral nucleus decreased inhibition causes increased excitement of the motor cortex which leads to increased movement so let's draw this out so we start up here in the motor cortex which then sends signals to the striatum so the caudate right here and the retainment right there the neurotransmitter released into the striatum is glutamate now this is an excitatory neurotransmitter which is why these arrows are green as in go so now the putamen is activated and it releases gaba which acts on the Globus pallidus internus as you can see right here now gaba is inhibitory hence the red arrow now the Globus pallidus internus normally inhibits the thalamus by releasing GABA specifically at the ventrolateral nucleus I'll just write VL the nuclei of the thalamus which include the VL are important and they are discussed in the thalamus lecture of this chapter so what's important to recognize is that because of the activation of the putamen the Globus pallidus internus is inhibited by gaba which means that its effect is inhibited which means there is increased excitement from the thalamus going to the motor cortex so this is the gist of the direct pathway or excitatory pathway the putamen has inhibited the inhibitor which is the Globus pallidus internus so now let's talk about the indirect or inhibitory pathway and the indirect or inhibitory pathway decreases movement so a signal starts in the motor cortex and then stimulates the striatum the caudate and the putamen and then gaba is released which causes increased inhibition of the Globus pallidus extranet which then causes decreased inhibition of the subthalamic nucleus which causes increased stimulation of the Globus pallidus internus as we recall from the direct pathway the Globus pallidus internus inhibits the thalamus so there is decreased stimulation of the thalamus again acting on the ventral lateral nucleus within the thalamus greater inhibition of the thalamus means that there is decreased excitement of the motor cortex which ultimately leads to decreased movement so let's draw this out so now we're focusing on the other half of figure 8.1 from your text so motor stimulation comes to the striatum as we discussed with the direct pathway goes to the caudate and it also goes to the putamen the patanè 'men is stimulated to release GABA into the Globus pallidus external which is clearly labeled on this left half so start right there so GABA is released and the Globus pallidus external is inhibited normally the Globus pallidus external inhibits the subthalamic nucleus right here so it would release GABA however with the stimulation of the / Taemin which causes the inhibition of the Globus pallidus external so the activity of the subthalamic nucleus is increased and as you can see there's a green arrow going from the subthalamic nucleus to the Globus pallidus internus and as we recall from the direct pathway the Globus pallidus internus actually inhibits the thalamus so the point is is that in the indirect pathway the motor cortex has stimulated to pooh taemin which then inhibits the inhibitor of the Globus pallidus internus so the Globus pallidus internus can be activated which leads to inhibition of the thalamus which actually means there is decreased stimulation of the motor cortex and therefore decreased movement so now let's talk about how to rock the basal ganglia questions on step one so the first thing you need to know is know the anatomical locations of each component of the basal ganglia so namely the caudate and putamen and also know the Globus pallidus and the thalamus on the left is figure eight point seven from your text showing an axial cut of the brain this was discussed in section one of this chapter on the right is figure eight point five from your text showing a coronal cut which we showed previously in this lecture now be sure to identify every element of the basal ganglia in each of these images so on the Left we have the caudate nucleus right here and we have the putamen right here we have the Globus pallidus external and Globus pallidus internus and on the right we have the caudate nucleus right here and we have the putamen right here and we have the Globus pallidus extras and internists now with a sagittal cut of the brain looking at figure eight point four from your text which was discussed in section one of this chapter we can identify once again be caudate right here which curves around the putamen right here and then just medial to that is the Globus pallidus which would be in here which is not easily visible from this perspective so now let's talk about the other portion of rocking your basal ganglia questions which is knowing the lesions the first thing you need to know is that damage to the subthalamic nucleus leads to hemi baalism or hemiballismus next know that damage to the striatum or the caudate and putamen leads to huntington disease also it's really important to know that unilateral lesions cause contralateral signs and we'll explain what we mean by all of this here's the full image of figure 8.3 one from your text and notice that if you damage the subthalamic nucleus you will cause dysfunction of the indirect pathway so you will see signs of lack of inhibition because remember that the indirect pathway decreases motor cortex stimulation which decreases movement so if you decrease the indirect pathway you will actually increase motor cortex stimulation and increase movement which leads to wild flailing movements known as hemiballismus so remember whenever you get damage to the subthalamic nucleus you're going to get hemi business which is the wild flailing movements the next point is that unilateral lesions will cause contralateral signs so on this side we have the patient's left and on this side we have the patient's right so if we damage any part of the right side of the basal ganglia we would only get signs on the left side of the body the reason is because the basal ganglia is responsible for modulating the motor cortex and as you recall from section two on the spinal tracts specifically regarding the corticospinal system the motor cortex will send fibers through the internal capsule which then decussate at the medulla so damage to any part of the right basal ganglia will be manifest with left-sided symptoms so the last point to make about the basal ganglia is regarding Huntington's disease I'll just write HD Huntington's disease is a hereditary disease which damages the striatum so both the caudate and the putamen so this will damage both the direct and indirect pathways after all both the caudate and putamen are involved in both the direct and indirect pathways as seen on this image recall that the indirect pathway is mainly inhibitory while the direct pathway is mainly excitatory so in Huntington's disease we are affecting both the excitatory component of the basal ganglia as well as the inhibitory component of the basal ganglia so damage to the indirect pathway will cause loss of inhibition so we'll have decreased inhibition which leads to the cortex being over stimulated which results in the jerky movements known as Korea in Huntington's disease conversely where the direct pathway is mainly excitatory and we actually have decreased excitement patients with patients with Huntington's disease will actually demonstrate that decreased slow movement so the slow movement and these jerky chorea movements are both known to be in Huntington's disease so let's do a question to apply this so let's say a 27 year old female patient presents with rapid involuntary movements in both arms now she was adopted and is unable to provide an adequate family history from the image below what region of the brain is likely damaged so here we're looking at the basal ganglia so with these symptoms and given the fact that we know that because of the question stem our patient has something wrong at the basal ganglia we should be thinking of one of two things first Huntington's disease and second hemiballismus so the rapid involuntary movements should make you think of the Curia in Huntington's disease so since we are thinking about Huntington's disease we would think that the striatum is damaged so the caudate and putamen on both sides now the reason we're not thinking it's hemiballismus is because if this patient had Hemi baalism we would see more of a wild flailing on one side of the body which is really not what we're seeing here however if we were thinking this patient had hemiballismus we'd be thinking of damage to the subthalamic nucleus and it would have to be in both sides because this patient is demonstrating symptoms in both arms again that's not what this patient's demonstrating so we're thinking it's Huntington's disease so now let's talk about the dopaminergic pathways now the dopaminergic pathways project axons to various locations in the brain to deliver dopamine now there are four major pathways the nigrostriatal the mesial limbic the musical cortical and finally the two baroque infundibular now this is figure 8.3 - from your text which shows all four dopaminergic pathways we are going to go through each pathway on this image one by one so don't worry about memorizing it now for now just focus on the midbrain if we took an axial cut of the midbrain like this we would see figure eight point 16 which was discussed in section 3 of this chapter notice how we can see the ventral tegmental area and the substantia the ventral tegmental area houses the cell bodies for the Meisel limbic and missoula cortical paths and the substantia houses the cell bodies for the Niagara striatal pathway if you remember these two areas the ventral tegmental area and the substantia it will make understanding the dopaminergic pathways so much easier so let's start with the nigrostriatal pathway so the substantia is divided into two parts the part we're concerned about is the pars compacta hence the see in this SN C now this releases dopamine which travels to the striatum so the caudate and putamen hence the term Nigro as in substantia and striatal as in striatum now dopamine stimulates the d1 and d2 receptors found in both the putamen and the caudate and when the d1 receptor stimulated it causes the excitatory pathway to be stimulated which leads to increased movement now the d2 receptor stimulation causes the inhibitory pathway to be inhibited we have inhibited the inhibitory pathway which also leads to increased movement in other words the Niagara's trail of pathway stimulates movement via the basal ganglia so now let's look at our image of 8.32 so here we have the substantia in red we're gonna follow the Niagara straddle pathway which starts here in the midbrain recall this is the midbrain area and it goes all the way up until it reaches the Australian in this area now let's look back at figure 8.3 one to apply this to the basal ganglia so the negros straddle pathway can stimulate the d1 receptors to stimulate the excitatory pathway so there are d1 receptors in the caudate and the putamen so the substantia on both sides will stimulate the direct pathway by stimulating the d1 receptors which causes increased activity of the direct pathway at the same time dopamine stimulates the d2 receptors which are also in the caudate and now when the substantia stimulates the d2 receptor in the inhibitory pathway it will cause decreased inhibition so in other words we will have decreased activity of the indirect pathway so ultimately the Niagra straddle pathway leads to increased movement so now let's do a question to apply this now what symptoms would you expect with damage to the substantia okay with damage to the substantia there would be loss of stimulation of the d1 and d2 receptors therefore there will be a less excitement of the basal ganglia and the motor cortex so the patient will present with decreased movement or specifically slow movement so what we are talking about here with damage to the substantia is Parkinson's disease so we can expect all the same symptoms of Parkinson's disease including poor posture and tremors which we can attribute to lack of stimulation of the d1 and d2 receptors in the striatum so now let's talk about the mesial limbic pathway in the mesial limbic pathway the ventral tegmental area which is in the midbrain releases dopamine the dopamine then travels to the nucleus accumbens which is a part of the limbic system and also travels to other structures within the limbic system so it can be easy to remember what the mesial limbic pathway is when we remember that the midbrain is also called the mesencephalon as in mezzo in Muzo limbic and since we're dealing with the limbic system we get the term limbic in missoula limbic pathway now the nucleus accumbens is the reward center of the brain and it's associated with drugs addictions food sex and other things like that when you have hyperactivity of the nucleus accumbens you get the positive symptoms of schizophrenia which include delusions and hallucinations now the muse or cortical pathway is very similar in that we can remember that it begins in the ventral tegmental area which is in the midbrain which is also called the mesencephalon as meesa for me so cortical pathway and just like in the Meisel limbic pathway the music cortical pathway has dopamine which travels to the prefrontal cortex hence the term cortical in music cortical pathway now the prefrontal cortex is responsible for motivation emotion and executive functions and when you have decreased activity or hypo activity of the music cortical pathway you get the negative symptoms associated with schizophrenia which include flat effect and head onea a volition and other things so now the last pathway is the tubero infundibular pathway in this pathway the hypothalamus releases dopamine which travels to the anterior pituitary which then inhibits the release of prolactin so if you have dysfunction of this pathway you're going to have decreased inhibition which causes increased serum prolactin when you have hyperprolactinemia you will get decreased libido khalaqtu Riya and other things so now looking again at figure 8.3 - we have the tubero infundibular pathway going from the hypothalamus in this region to the anterior pituitary and as we mentioned in the previous slide when we damage the tubero infundibular pathway we get decreased dopamine which causes decreased inhibition of prolactin secretion which of course leads to hyper prolactin emia for more information about prolactin secretion please watch the endocrine chapter so now let's review all of the dopaminergic pathways together recall that they all project axons to various locations in the brain to deliver dopamine there are four major pathways the Niagra straddle which goes from the substantia to the striatum and if you have destruction of this you get Parkinson's disease and the mesial limbic pathway goes from the mesencephalon or midbrain specifically the ventral tegmental area to the olympic system and when you have hyperactivity of this system you get the positive symptoms associated with schizophrenia and the mesial cortical goes from ventral tegmental area to the prefrontal cortex when this is hypoactive you get the negative symptoms associated with schizophrenia and finally as we just reviewed on the previous slide the tubero infundibular pathway is responsible for inhibiting the release of prolactin so when it's hypoactive you will get hyperprolactinemia now if you can remember these four pathways their locations and what happens if they are dysfunctional as written here you will do quite well on any question you'll get regarding these pathways so let's just do one last question to review what pathway is affected causing a flat effect in a schizophrenic patient so to answer this question you just need to think about what dopaminergic pathway is responsible for emotion and motivation now that would be the prefrontal cortex and that means that we're dealing with the mezzo cortical pathway as you recall the prefrontal cortex is responsible for emotion and motivation if you have dysfunction of this pathway you're going to have decreased emotion and motivation which gives you those negative symptoms associated with schizophrenia as a side note recall that when dealing with the Meisel limbic pathway here in green when you get this hyperactive you're actually going to get increased activity of the limbic system including the nucleus accumbens which causes those positive symptoms associated with schizophrenia when you have a problem with the Nyiro striatal pathway or damage to the substantia you're going to get Parkinson's like symptoms or Parkinson's disease and when you think to burrow infundibulum problem think hyperprolactinemia and that concludes this section

welcome to section six in Neurology in this section we will be discussing the basal ganglia and the dopaminergic pathways so let's get started so the basal ganglia is responsible for smooth voluntary movements it's composed of the striatum which is composed of the caudate and putamen and the lenta form which is composed of the per Taemin and Globus pallidus it also has the substantia pars compacta and a c4 compacta and also has the subthalamic nucleus or stn for short now the basal ganglia contains the direct pathway which increases movement as well as the indirect pathway which decreases movement so now let's show some anatomy of these locations here is a sagittal view of the brain this is actually figure 8.4 which was discussed in section 1 of this chapter what I would like to have you focus on now is the basal ganglia as you can see the caudate is here it actually extends back and then it curves forward again and then we have the per Taemin which as this line indicates is right here and just medial to that is the thalamus as you can see here now the Globus pallidus is actually medial to the Petain 'men and you can't really visualize it here but if we were to take a coronal section of the brain and cut it through this portion we would see figure eight point five figure eight point five was also discussed in section one of this chapter so now we can see that the caudate nucleus is located here and that the thalamus is located here and then of course we have the / Taemin right in this region and the Globus pallidus external and then the Globus pallidus internus now let's show a slightly more posterior coronal cut of the brain on a new slide since we are more posterior than in figure eight point five shown in the previous slide we can see the brainstem right here and the substantia in the midbrain as we will discuss later in this lecture the substantia plays an important in the basal ganglia as discussed in section 3 of this chapter the red nucleus is also in the midbrain right here and right here and is the red nucleus and we will discuss the relevance of knowing that the substantia and the red nucleus are located in the midbrain once we get later in this lecture and discuss the dopaminergic pathways so now that we have our landmarks let's discuss the direct and indirect pathways of the basal ganglia so on the Left we have demonstrated the direct pathway and on the right we've demonstrated the indirect pathway it's important to recognize that both the indirect and direct pathways are on both sides of the brain but for simplicity in this lecture we will illustrate the indirect and direct pathways separately on separate parts of the brain so now let's first discuss the direct pathway so the direct pathway is the excitatory pathway which means it increases movement and the pathway starts in the motor cortex which then stimulates the striatum specifically the caudate and the putamen at which point the neurotransmitter gaba is released and then we'll see inhibition of the Globus pallidus internus which causes decreased inhibition of the thalamus specifically acting on the ventral lateral nucleus decreased inhibition causes increased excitement of the motor cortex which leads to increased movement so let's draw this out so we start up here in the motor cortex which then sends signals to the striatum so the caudate right here and the retainment right there the neurotransmitter released into the striatum is glutamate now this is an excitatory neurotransmitter which is why these arrows are green as in go so now the putamen is activated and it releases gaba which acts on the Globus pallidus internus as you can see right here now gaba is inhibitory hence the red arrow now the Globus pallidus internus normally inhibits the thalamus by releasing GABA specifically at the ventrolateral nucleus I'll just write VL the nuclei of the thalamus which include the VL are important and they are discussed in the thalamus lecture of this chapter so what's important to recognize is that because of the activation of the putamen the Globus pallidus internus is inhibited by gaba which means that its effect is inhibited which means there is increased excitement from the thalamus going to the motor cortex so this is the gist of the direct pathway or excitatory pathway the putamen has inhibited the inhibitor which is the Globus pallidus internus so now let's talk about the indirect or inhibitory pathway and the indirect or inhibitory pathway decreases movement so a signal starts in the motor cortex and then stimulates the striatum the caudate and the putamen and then gaba is released which causes increased inhibition of the Globus pallidus extranet which then causes decreased inhibition of the subthalamic nucleus which causes increased stimulation of the Globus pallidus internus as we recall from the direct pathway the Globus pallidus internus inhibits the thalamus so there is decreased stimulation of the thalamus again acting on the ventral lateral nucleus within the thalamus greater inhibition of the thalamus means that there is decreased excitement of the motor cortex which ultimately leads to decreased movement so let's draw this out so now we're focusing on the other half of figure 8.1 from your text so motor stimulation comes to the striatum as we discussed with the direct pathway goes to the caudate and it also goes to the putamen the patanè 'men is stimulated to release GABA into the Globus pallidus external which is clearly labeled on this left half so start right there so GABA is released and the Globus pallidus external is inhibited normally the Globus pallidus external inhibits the subthalamic nucleus right here so it would release GABA however with the stimulation of the / Taemin which causes the inhibition of the Globus pallidus external so the activity of the subthalamic nucleus is increased and as you can see there's a green arrow going from the subthalamic nucleus to the Globus pallidus internus and as we recall from the direct pathway the Globus pallidus internus actually inhibits the thalamus so the point is is that in the indirect pathway the motor cortex has stimulated to pooh taemin which then inhibits the inhibitor of the Globus pallidus internus so the Globus pallidus internus can be activated which leads to inhibition of the thalamus which actually means there is decreased stimulation of the motor cortex and therefore decreased movement so now let's talk about how to rock the basal ganglia questions on step one so the first thing you need to know is know the anatomical locations of each component of the basal ganglia so namely the caudate and putamen and also know the Globus pallidus and the thalamus on the left is figure eight point seven from your text showing an axial cut of the brain this was discussed in section one of this chapter on the right is figure eight point five from your text showing a coronal cut which we showed previously in this lecture now be sure to identify every element of the basal ganglia in each of these images so on the Left we have the caudate nucleus right here and we have the putamen right here we have the Globus pallidus external and Globus pallidus internus and on the right we have the caudate nucleus right here and we have the putamen right here and we have the Globus pallidus extras and internists now with a sagittal cut of the brain looking at figure eight point four from your text which was discussed in section one of this chapter we can identify once again be caudate right here which curves around the putamen right here and then just medial to that is the Globus pallidus which would be in here which is not easily visible from this perspective so now let's talk about the other portion of rocking your basal ganglia questions which is knowing the lesions the first thing you need to know is that damage to the subthalamic nucleus leads to hemi baalism or hemiballismus next know that damage to the striatum or the caudate and putamen leads to huntington disease also it's really important to know that unilateral lesions cause contralateral signs and we'll explain what we mean by all of this here's the full image of figure 8.3 one from your text and notice that if you damage the subthalamic nucleus you will cause dysfunction of the indirect pathway so you will see signs of lack of inhibition because remember that the indirect pathway decreases motor cortex stimulation which decreases movement so if you decrease the indirect pathway you will actually increase motor cortex stimulation and increase movement which leads to wild flailing movements known as hemiballismus so remember whenever you get damage to the subthalamic nucleus you're going to get hemi business which is the wild flailing movements the next point is that unilateral lesions will cause contralateral signs so on this side we have the patient's left and on this side we have the patient's right so if we damage any part of the right side of the basal ganglia we would only get signs on the left side of the body the reason is because the basal ganglia is responsible for modulating the motor cortex and as you recall from section two on the spinal tracts specifically regarding the corticospinal system the motor cortex will send fibers through the internal capsule which then decussate at the medulla so damage to any part of the right basal ganglia will be manifest with left-sided symptoms so the last point to make about the basal ganglia is regarding Huntington's disease I'll just write HD Huntington's disease is a hereditary disease which damages the striatum so both the caudate and the putamen so this will damage both the direct and indirect pathways after all both the caudate and putamen are involved in both the direct and indirect pathways as seen on this image recall that the indirect pathway is mainly inhibitory while the direct pathway is mainly excitatory so in Huntington's disease we are affecting both the excitatory component of the basal ganglia as well as the inhibitory component of the basal ganglia so damage to the indirect pathway will cause loss of inhibition so we'll have decreased inhibition which leads to the cortex being over stimulated which results in the jerky movements known as Korea in Huntington's disease conversely where the direct pathway is mainly excitatory and we actually have decreased excitement patients with patients with Huntington's disease will actually demonstrate that decreased slow movement so the slow movement and these jerky chorea movements are both known to be in Huntington's disease so let's do a question to apply this so let's say a 27 year old female patient presents with rapid involuntary movements in both arms now she was adopted and is unable to provide an adequate family history from the image below what region of the brain is likely damaged so here we're looking at the basal ganglia so with these symptoms and given the fact that we know that because of the question stem our patient has something wrong at the basal ganglia we should be thinking of one of two things first Huntington's disease and second hemiballismus so the rapid involuntary movements should make you think of the Curia in Huntington's disease so since we are thinking about Huntington's disease we would think that the striatum is damaged so the caudate and putamen on both sides now the reason we're not thinking it's hemiballismus is because if this patient had Hemi baalism we would see more of a wild flailing on one side of the body which is really not what we're seeing here however if we were thinking this patient had hemiballismus we'd be thinking of damage to the subthalamic nucleus and it would have to be in both sides because this patient is demonstrating symptoms in both arms again that's not what this patient's demonstrating so we're thinking it's Huntington's disease so now let's talk about the dopaminergic pathways now the dopaminergic pathways project axons to various locations in the brain to deliver dopamine now there are four major pathways the nigrostriatal the mesial limbic the musical cortical and finally the two baroque infundibular now this is figure 8.3 - from your text which shows all four dopaminergic pathways we are going to go through each pathway on this image one by one so don't worry about memorizing it now for now just focus on the midbrain if we took an axial cut of the midbrain like this we would see figure eight point 16 which was discussed in section 3 of this chapter notice how we can see the ventral tegmental area and the substantia the ventral tegmental area houses the cell bodies for the Meisel limbic and missoula cortical paths and the substantia houses the cell bodies for the Niagara striatal pathway if you remember these two areas the ventral tegmental area and the substantia it will make understanding the dopaminergic pathways so much easier so let's start with the nigrostriatal pathway so the substantia  is divided into two parts the part we're concerned about is the pars compacta hence the see in this SN C now this releases dopamine which travels to the striatum so the caudate and putamen hence the term Nigro as in substantia and striatal as in striatum now dopamine stimulates the d1 and d2 receptors found in both the putamen and the caudate and when the d1 receptor stimulated it causes the excitatory pathway to be stimulated which leads to increased movement now the d2 receptor stimulation causes the inhibitory pathway to be inhibited we have inhibited the inhibitory pathway which also leads to increased movement in other words the Niagara's trail of pathway stimulates movement via the basal ganglia so now let's look at our image of 8.32 so here we have the substantia in red we're gonna follow the Niagara straddle pathway which starts here in the midbrain recall this is the midbrain area and it goes all the way up until it reaches the Australian in this area now let's look back at figure 8.3 one to apply this to the basal ganglia so the negros straddle pathway can stimulate the d1 receptors to stimulate the excitatory pathway so there are d1 receptors in the caudate and the putamen so the substantia on both sides will stimulate the direct pathway by stimulating the d1 receptors which causes increased activity of the direct pathway at the same time dopamine stimulates the d2 receptors which are also in the caudate and now when the substantia stimulates the d2 receptor in the inhibitory pathway it will cause decreased inhibition so in other words we will have decreased activity of the indirect pathway so ultimately the Niagra straddle pathway leads to increased movement so now let's do a question to apply this now what symptoms would you expect with damage to the substantia okay with damage to the substantia there would be loss of stimulation of the d1 and d2 receptors therefore there will be a less excitement of the basal ganglia and the motor cortex so the patient will present with decreased movement or specifically slow movement so what we are talking about here with damage to the substantia is Parkinson's disease so we can expect all the same symptoms of Parkinson's disease including poor posture and tremors which we can attribute to lack of stimulation of the d1 and d2 receptors in the striatum so now let's talk about the mesial limbic pathway in the mesial limbic pathway the ventral tegmental area which is in the midbrain releases dopamine the dopamine then travels to the nucleus accumbens which is a part of the limbic system and also travels to other structures within the limbic system so it can be easy to remember what the mesial limbic pathway is when we remember that the midbrain is also called the mesencephalon as in mezzo in Muzo limbic and since we're dealing with the limbic system we get the term limbic in missoula limbic pathway now the nucleus accumbens is the reward center of the brain and it's associated with drugs addictions food sex and other things like that when you have hyperactivity of the nucleus accumbens you get the positive symptoms of schizophrenia which include delusions and hallucinations now the muse or cortical pathway is very similar in that we can remember that it begins in the ventral tegmental area which is in the midbrain which is also called the mesencephalon as meesa for me so cortical pathway and just like in the Meisel limbic pathway the music cortical pathway has dopamine which travels to the prefrontal cortex hence the term cortical in music cortical pathway now the prefrontal cortex is responsible for motivation emotion and executive functions and when you have decreased activity or hypo activity of the music cortical pathway you get the negative symptoms associated with schizophrenia which include flat effect and head onea a volition and other things so now the last pathway is the tubero infundibular pathway in this pathway the hypothalamus releases dopamine which travels to the anterior pituitary which then inhibits the release of prolactin so if you have dysfunction of this pathway you're going to have decreased inhibition which causes increased serum prolactin when you have hyperprolactinemia you will get decreased libido khalaqtu Riya and other things so now looking again at figure 8.3 - we have the tubero infundibular pathway going from the hypothalamus in this region to the anterior pituitary and as we mentioned in the previous slide when we damage the tubero infundibular pathway we get decreased dopamine which causes decreased inhibition of prolactin secretion which of course leads to hyper prolactin emia for more information about prolactin secretion please watch the endocrine chapter so now let's review all of the dopaminergic pathways together recall that they all project axons to various locations in the brain to deliver dopamine there are four major pathways the Niagra straddle which goes from the substantia to the striatum and if you have destruction of this you get Parkinson's disease and the mesial limbic pathway goes from the mesencephalon or midbrain specifically the ventral tegmental area to the olympic system and when you have hyperactivity of this system you get the positive symptoms associated with schizophrenia and the mesial cortical goes from ventral tegmental area to the prefrontal cortex when this is hypoactive you get the negative symptoms associated with schizophrenia and finally as we just reviewed on the previous slide the tubero infundibular pathway is responsible for inhibiting the release of prolactin so when it's hypoactive you will get hyperprolactinemia now if you can remember these four pathways their locations and what happens if they are dysfunctional as written here you will do quite well on any question you'll get regarding these pathways so let's just do one last question to review what pathway is affected causing a flat effect in a schizophrenic patient so to answer this question you just need to think about what dopaminergic pathway is responsible for emotion and motivation now that would be the prefrontal cortex and that means that we're dealing with the mezzo cortical pathway as you recall the prefrontal cortex is responsible for emotion and motivation if you have dysfunction of this pathway you're going to have decreased emotion and motivation which gives you those negative symptoms associated with schizophrenia as a side note recall that when dealing with the Meisel limbic pathway here in green when you get this hyperactive you're actually going to get increased activity of the limbic system including the nucleus accumbens which causes those positive symptoms associated with schizophrenia when you have a problem with the Nyiro striatal pathway or damage to the substantia you're going to get Parkinson's like symptoms or Parkinson's disease and when you think to burrow infundibulum problem think hyperprolactinemia and that concludes this section

Transcript for:Understanding Basal Ganglia and Pathways

Transcript for:
Understanding Basal Ganglia and Pathways