Migraine Medications

what's up ninja nerds in this video today we're going to be talking about the pharmacology of migraine medications before we get started it's super important that if you guys really do enjoy this video you like it it helps you support us and the best way that you can support us is by hitting that subscribe button hitting the like button and commenting down in the comment section all right insurance let's get into it all right ninja so when we talk about migraine medications before we start getting into the names of them their mechanism of action when we use them all that stuff like that let's briefly and quickly go through the pathophysiology of migraines because if we understand that the mechanism of action all that stuff is going to make so much sense so really really quickly and briefly whenever someone develops a migraine there's really this kind of irritation and agitation and activation of particular types of noisy acceptors or trigeminal nerves that are occurring that are present within the meninges you know within the meninges you have like the dura mater and so what happens is whenever someone develops a migraine these noisy acceptors that are within the dura mater right here we're just taking this part here and zooming in on it they can become activated and irritated and start releasing particular types of neurotransmitters or molecules and these molecules include vaso active peptide another one includes substance p and the other one is called calcitonin gene regulated peptide and that's c g r p either way when these three chemicals are released they can do three particular things one is they can come over here and they can act on these cells here called mast cells you know mast cells they contain lots of you know granules that whenever they degranulate and release some of these particular chemicals within those granules what do they release well they can release molecules like histamines you know histamines what they love to do they love to act on the vascular smooth muscle and induce what type of process they love to induce vasodilation and what is that called that's basically whenever the the vet the vessels become bigger right more plumper they open up their diameter increases all of the above right the other thing histamines can do is besides causing vasodilation is they can also kind of increase the spaces between the endothelial cells what's that called when you increase the spaces between the endothelial cells and allow more things to leak out it increases the capillary permeability baby so these are kind of two things so that allows a lot of like proteins to extravaze out of the blood vessel the other thing is not only does it release histamines but it also releases another molecule which can kind of do the same kind of effect and these are your prostaglandins right so your prostaglandins and these can kind of produce somewhat of this similar effect as we just mentioned here so that's one kind of mechanism right so the first one is we can stimulate mast cells and kind of stimulate this inflammatory reaction causing vasodilation increasing vascular permeability the other thing that we can do is that these chemicals can do that directly so they can literally do the same kind of mechanism but they can do it directly by acting on those vessels and increasing the release of other types of molecules like nitric oxide that trigger the same kind of response either way whenever there's this vasodilation this increased capillary permeability a lot of inflammatory mediators all of these things lead to the activation of these particular types of other nearby noisy acceptors that are connected to or associated with a very particular cranial nerve and this cranial nerve is called cranial nerve five the trigeminal nerve when these noisy acceptors of cranial nerve five are activated because of this vasodilation increased capillary permeability and a lot of inflammatory reactions here as well as the third thing is that sometimes these chemicals can also act on these noisy acceptors directly and stimulate them whenever these cranial nerves are activated whenever the noisy receptors of cranial nerve 5 are activated it sends action potentials down the afferent fibers of that trigeminal nerve to the trigeminal nucleus what is this called this is the trigeminal nucleus located within the brainstem from here it'll send this information up to a structure which is the relay station for all sensory information going to the cerebral cortex called your thalamus and then your thalamus will tell your cerebral cortex hey buddy there's some kind of pain sensation coming from the trigeminal nerve due to these inflammatory mediators that are being released from these actual noisy acceptors that were activated for some reason we don't know why but that occurred and you know we know that the trigeminal nerve is activated well the trigeminal nerve what we know about this is kind of its sensory distribution right the big thing here is the trigeminal nerve picks up sensation from the head right so if we're picking up sensation from like the orbital region or the supraorbital region or the temporal region or the frontal region all of that stuff is getting traveled down through the trigeminal nerve and then to the central nervous system so what we the trigeminal nerve does is it picks up sensations of the face and so that pain sensation that we are experiencing because of this neurogenic inflammation is getting sent down the trigeminal nerve and taken to the cortex so we feel pain but it's in the vicinity of the orbital region the supraorbital region the frontal region and the temporal region and this produces the classic headache presentation that you see with a migraine okay now there's one other thing that i want to talk about migraines can also present with auras right so auras are basically there's this theory called the cortical spreading depression theory where there is a depolarization wave that travels over the cortex for some reason so this thought of auras which again auras are basically whenever someone usually it's when someone has like visual kind of abnormal abnormalities or they see sparkling lights like scotomas scintillating scotoma centroscotomas they see like fortification spectra basically abnormal visual things that precede the headache that they're going to experience maybe they even have abnormal smells or sensations or weakness on one side but either way the theory behind someone developing an aura was postulated and it's theoretical that maybe this has something to do with serotonin okay and whenever someone has an aura what we notice is that their serotonin levels seem to be higher for some reason and if their serotonin levels are higher these act on particular serotonin receptors five ht1 receptors on blood vessels and induce vasoconstriction of that blood vessel now when these blood vessels clamp down and cause that kind of vasoconstriction mechanism that's what's believed to be triggering this kind of aura process but when someone what they also found is that when people are actually experiencing the headache part of the migraine without any kind of aura there's lower levels of 5-hydroxytryptomy serotonin and so if there's lower levels of that it's not binding onto these actual 5-ht-1 receptors as often not triggering them to contract and so instead if there's less amounts of that serotonin present these vessels will undergo vasodilation and if you remember what did vasodilation and increased capillary permeability do it caused this neurogenic inflammation stimulated the noisy acceptors of cranial nerve five sent that information into the trigeminal system up to the thalamus up to the sensory cortex and lead to the perception of pain so there's this theory or epiphenomenon that maybe there can be lower levels of serotonin that are triggering vasodilation mechanisms which may be a potential trigger or cause for neurogenic inflammation and causing these migraines all right so what i want to do is quickly recap before we talk about acute and prophylactic therapy here when i'm talking about migraines again you got to remember that that trigeminal ganglion if you guys remember your anatomy it's kind of located outside of your central nervous system and then has these divisions your v1 your v2 your v3 divisions right so v1 v2 and v3 division which go and supply parts of the head which we just we annotated here right well if you remember these are sensory fibers so if we had like at the end of these maybe there was some noisy acceptors it's our pain receptors so they're picking up pain stimulus from whatever reason what were the particular reasons we said that we could stimulate noise receptors of the trigeminal nerve it was either due to an increase in cgrp an increase in substance p an increase in vasoactive peptide or a decrease in 5-hydroxytryptamine either way by some way shape or form these were causing vasodilation of the vessels increased vascular permeability or histamine and prostaglandin release activating those noisy acceptors and sending those fibers down the afferent component of that trigeminal nerve to the actual ganglion from the ganglion this will get sent in to your actual brainstem where it'll go to the trigeminal nuclei within the brainstem from there it'll then get sent up to the thalamus and then from the thalamus that'll get sent up to your sensory cortex and you'll become aware consciously aware of the pain within the different divisions of the actual trigeminal nerve system which is within the head region and so that's where the pain from the headaches actually comes from all right so when we're trying to treat someone for migraines what we're trying to target in these patients is the particular types of molecules here like cgrp we'll have some particular drugs that target that we also have drugs that target the vasoactive peptide we have drugs that target particularly modulate the activity of 5-hydroxytryptamine and what's not mentioned here is that if there's a particular trigger and will represent that hair in green is that a lot of this is inflammatory so if we can also give drugs that are going to reduce inflammation that will also be beneficial in these patients so when we're having a person coming in with an acute kind of migraine right our treatment therapy is geared towards what well the first thing is let's reduce inflammation so this is where things like nsaids can become pretty beneficial the second thing is let's give drugs that really help to increase the serotonin concentration and the first line drug there is going to be your tryptans the second line drug is going to be what's called your ergots and we'll discuss those and then the fourth thing that we can also add on here is again modulating that inflammation but it's not through nsaids it's through steroids and so utilizing particular types of steroids may also be beneficial in this scenario for prophylactic therapy in patients who have chronic migraines and we're trying to prevent them from developing future migraines this is where we'll give drugs that really target again they may work in some unknown mechanism we're not quite sure how but there's drugs that are like what's called propanol panel law or metoprolol which are beta blockers their second one which could be like anti-convulsants and these would be very important to remember as well things like to pyramid so you can remember to pyramid as well as valproate and again the way that these drugs work isn't completely worked out yet the third thing is we do have some drugs that may be actually able to inhibit cgrp and so we can use drugs called cgrp antagonists and then lastly we can give actual drugs that block pain sensation and so when we give drugs which are called the botox a injections these actually block the pain sensations that are picked up via the trigeminal nerve system okay so we got the pathophysiology down and what we're going to start with which is our acute therapy and our prophylactic therapy now let's talk about the different names of drugs and how these drugs actually work all right ninjas now that we nailed down our pathophys this should be so easy and so quick to understand the mechanism of action while we're going through the mechanism of action of these drugs we'll mention their name so that we can help to remember these so the first one is tryptance so tryptans are actually very interesting and you know what's nice about these drugs there's a couple different types for these ones so you have what's called suma tryptan and zoma tryptan and again these are the most commonly ones common wants to remember but any time you see again it's not very hard to remember a drug that ends in tryptan that's going to be a triptan type of drug now what do i want you to know about these drugs now these drugs can be given in a couple different forms they can be given po all right so they can be given oral they also can be given intranasal they can be given subcutaneously so we can give these in various different forms but what i want you to know is that tryptans they work via the serotonin receptors but very specific types so five ht one receptors but two subtypes type b and type d and so let's imagine here this is the sarah the tryptan drug what it's gonna do is it's going to bind onto these serotonin type 1 b and d receptors when it does that guess what it does it inhibits the vesicles from releasing a very particular types of chemicals what chemicals do you think are going to be released from this actual neuron this noisy receptive trigeminal neuron it's going to release molecules like we'll abbreviate them vaso active peptide substance p and cgrp now if you do that and you inhibit these chemicals what was the overall effect of that if you decrease the release of these then they won't act directly on the blood vessel and cause vasodilation and increased capillary permeability so you're going to inhibit that process and that process so now you're going to reduce inflammation in that aspect the other thing is if you don't have these chemicals that are going to be released you'll actually won't have these mast cells release as much histamines so there'll be a decrease in that and there also be a decrease in prostaglandins and if there's a decrease in histamines and a decrease in prostaglandins what does that mean that means that there's going to be a decrease in or inhibition of this vasodilation and increased vascular permeability if there is a decrease in that mechanism what's that going to do whenever there's this decreased neurogenic inflammation so there is a decrease in neuro genic inflammation by that process that is going to decrease or inhibit the activity of the stimulation of cranial nerve 5 the trigeminal nerve that means less signals are carried down that trigeminal nerve less is going to the trigeminal nucleus less is going to the thalamus and less is going to the cerebral cortex so the sensations that are usually carrying that pain signals due to this neurogenic inflammation is less so it decreases the headache doesn't that make sense yeah baby all right so that's one way that these drugs can work the second way that they can work is they can just also act on various cerebral blood vessels so if you imagine here the same kind of mechanism here is that you can also give these drugs not only will they inhibit the release of these substances but they will also these tryptans will also bind onto other 5-ht receptors on blood vessels and what will they do they'll inhibit this vasodilation mechanism what's the opposite of vasodilation it'll cause vasoconstriction so it'll induce vasoconstriction of these actual vessels and that'll help to again reduce that neurogenic inflammation reduce the activation of the trigeminal nerve reduced the pain signaling to the cerebral cortex oh maybe we done made sense of it all right so again tryptans you got sumatriptan zomatriptan they block the 5ht1 bd receptors inhibit the release of these peptides which inhibit histamine prostaglandin release inhibit vasodilation increase vascular permeability and result decrease neurogenic inflammation by decreasing the neurogenic inflammation instead of them causing vasodilation they actually cause vasoconstriction whether it be indirectly through inhibiting these peptides or directly and then that decreases the signaling down that trigeminal nerve decreasing the pain pathway all right beautiful what about ergots guess what ergots do the exact same dang thing it's just they bind on to way more different types of 5-ht receptors so ergots these are ergot alkaloids and the particular one that i want you to know is called dye dihydro ergotamine and again this one can be given po but it can also be given iv im sub q you can even give it intranasally so this one is the second line agent after tryptan so tryptans are your first line in migraines ergots are the second line now these drugs also act on 5ht receptors but guess what they work on all of them they aren't specific they can work on any 5-ht receptor and you know why that's a problem we'll talk about a little bit later when we get into side effects there's 5 ht3 receptors on the chemo trigger zone in the brain stem guess what that causes when you stimulate it vomiting and so it can also act on a bunch of other structures too so remember it acts on all of that 5 ht receptors okay how do they work the same kind of mechanism we don't really need to go crazy into it it binds onto the 5 ht receptors inhibits the release of vasoactive peptide decreases the substance p release decreases cgrp that will then decrease the direct effect on the blood vessel which will inhibit vasodilation and instead lead to vasoconstriction as well as decreasing vascular permeability it will inhibit the mast cells from releasing histamines and prostaglandins to again decrease vasodilation and vascular permeability if you do all of those above things you decrease neurogenic inflammation decrease activation of the cranial nerve and you decrease the pain that you're feeling within that poor little head okay as well as ergots can also act directly on the blood vessels within the cerebrum and cause vasoconstriction of those blood vessels as well okay the only other thing to add on here is ergots can also bind on to alpha one receptors okay so whenever ergots bind onto alpha one receptors they can also induce vasoconstriction within the peripheral blood vessels as well so that's another big thing to remember they can induce pretty intense peripheral vasoconstriction okay so remember they also act on alpha-1 receptors besides the 5-ht all those receptors okay that covers the two big ones that i wanted you guys to remember for what for the acute therapy the other ones is your anti-inflammatories your nsaids and your steroids how do they work it's really simple and thank goodness they generally decrease a lot of this inflammatory reaction a lot of this kind of vasodilation mechanism a lot of the histamine prostaglandin release and so when i kind of just all we need to do is is take into consideration here nsaids right and there's so many different types of nsaids the commonly utilized ones are going to be like ibuprofen naproxen if you can take oral right if you can't take oral because you know sometimes when people have migraines they could be vomiting you may have to give another one called ketoralac these would be drugs that you would give and what they would do is they would just inhibit that prostaglandin release which would inhibit that neurogenic inflammation the other drug that you could give is certain types of steroids and steroids also reduce a lot of this inflammatory reaction as we stated above and the best one that we've seen here is dexamethasone so it's relatively easy when we break these down right the tryptans and the ergots are going to cause vasoconstriction and inhibit the release of those peptides which overall reduce neurogenic inflammation reduce signaling down that cranial nerve five nsaids and steroids reduce the neurogenic inflammation just by inhibiting the prostaglandin process and histamine process and still reducing neurogenic inflammation reducing the signals down that trigeminal nerve reducing the pain pathway we covered our acute therapy now what about the prophylactic therapy remember i told you one of the first line prophylactic medications are your beta blockers and there's two particular beta blockers that i want you guys to think about when we talk about beta blockers let's actually be specific and say beta2 but this consists of propranolol and metoprolol again these are prophylactic how do these drugs work well how they work is that they bind onto these beta 2 receptors present within the cerebral vessels now beta 2 receptors naturally want to cause vasodilation but if you're inhibiting that what are you going to do you're going to cause vasoco vasoconstriction right so that's what would happen with these normally beta-2 receptors will want to cause vasodilation so let's actually write that down beta-2 receptors naturally want to induce vasodilation but if you inhibit if you inhibit the beta-2 receptors this will cause the exact opposite of that which will induce vasoconstriction and again if we reduce vasoconstriction what's the overall kind of goal here is we're reducing a lot of that neurogenic inflammation okay all right so we covered so far the part of the prophylactic therapy we covered the beta blockers right propanol metoprolol now the anti-convulsants now the interesting thing about the anti-convulsants is that we don't really know how they actually help with migraines what their mechanism of action is it's kind of been you know not completely elucidated but again this consists of your to pyramid in your valproate what the theoretical thought is is that they're sodium channel blockers right so you have sodium channels that are present on the you know particularly on the axon and so if you inhibit if you use these drugs and inhibit these sodium channels you may decrease the action potentials that are traveling down the axon and then maybe decrease the release of cgrp which is again what was that drug called calcitonin gene regulated peptide right cgrp you may decrease substance p release and you may decrease the what else the vasoactive peptide release and the whole thought behind that is again these chemicals act on the mast cells and induce histamine release and prostaglandin release they act on the blood vessels directly and induce vasodilation and increase capillary permeability or they act on noisy acceptors and stimulate them basically inducing this neurogenic inflammation so if you give these drugs they may help in that process but it's not completely known the next ones that we got to think about here and again these are sometimes added in i didn't include this one it's kind of a second line agent after beta blockers and anticonvulsants is tricyclic antidepressants sometimes amitriptyline is utilized as a prophylactic agent how this drug works is kind of interesting so what the thought is is that remember i told you that with blood vessels whenever there is kind of this lower level of serotonin they undergo that vasodilation mechanism well if we give tricyclic antidepressants the thought is is that these may act to increase the concentration of 5-hydroxytryptamine and so if you increase the concentration of 5-hydroxytryptamine these will bind onto those a5ht receptors and induce vasoconstriction helping to reduce that neurogenic inflammation the next drug is your cgrp antagonist these ones should actually be the easiest one because their name is like directly there everywhere where the cgrp will bind it'll inhibit and inhibit the noise receptor activation inhibit the vasodilation increase capillary permeability and inhibit the histamine release basically it's going to work in all these three parts of that pathway right so this would be drugs like arynemab or um galcanizumab but really anything that ends in this map would kind of clue you into thinking about a cgrp antagonist okay the last one here is the botulinum toxin so the botulinum toxin particularly the type a botulinum toxin it's a very interesting kind of therapy here so again this is type a what it'll do is it'll actually work by kind of getting taken in to the synaptic vesicles getting taken into the synaptic terminal and basically inhibiting the release of a lot of these different pain signals so basically what it's going to do is it's going to decrease the pain signaling and that pain signaling is carried down trigeminal nerves so if you decrease the sensation that are getting carried down the actual trigeminal nerve that'll decrease the actual pain pathway and again what you do is you find different points injection points and inject where you think that the botulinum toxin would be very effective by again inhibiting or decreasing the pain signals of those noisy acceptors of the trigeminal nerve okay so that is the different types of drugs that we can use acutely or prophylactically and that is their mechanism of action let's talk about now the adverse effects and contraindications all right so now let's talk about the adverse effects and contraindications now when we talk about migraine medications the most important ones that i really wanted you to focus on within this video is your sumatriptan or your triptans in general sumatrift enzomotryptam so the triptan family your ergots like your dihydroargodamine and then the cgrp antagonist those are the big ones all the other ones that we mentioned we're not going to really go into those adverse effects because we'll talk about them in other videos and other disorders that they actually are treated for so let's focus most of our time for migraine medications adverse effects on tryptans ergots and we'll talk about cgrp antagonists briefly so tryptans what are the particular adverse effects well here's one of the big things that you got to think about what does it do to vessels not just in the cerebral vessels but it also does this on vessels of the heart other blood vessels within the systemic circulation so if it does this on blood vessels of the heart it causes vasoconstriction right so just let's write vasoconstriction so think about this if you cause a vasoconstriction of let's say the coronary vessels what could that lead to well that could lead to angina right that could lead to what's called prince metals that could lead to potentially worst case scenario a myocardial infarction so would you think that it would be a great idea to give a triptan to someone who already has prinze metals angina they have severe coronary artery disease or they have a history of a myocardial infarction probably not what if it can induce vasoconstriction of just your systemic vessels well what would that do well that could potentially increase your blood pressure leading to hypertension it could also clamp down on vessels that are going to maybe your actual extremities and lead to some actual peripheral vascular disease but actually let's be more specific it should really be peripheral artery disease right and so you got to think about that if someone has a history of peripheral artery disease that might not be a good medication to give to this patient or if they have severely high blood pressure it might not be a great idea to give that medication okay so that's something to think about for these what's another problem with this drug it actually may work by again altering some of the actual sensations that are carried via the nerves from the extremities and so it may present with potential paresthesias from our little dude right here okay or maybe some cold extremities okay some cold extremities all right boom let's move on the next thing that you have to remember here is that sometimes this can also induce some smooth muscle contraction so if it has the ability to induce contraction of smooth muscle and you got a baby bacon up in there would you want to pop that sucker out no so it's contraindicated in pregnancy so you would not want to give this break okay sorry so it's contraindicated gotcha so it's contraindicated in what kind of condition you'd want to have this definitely not give this drug to someone who is pregnant so contraindication in pregnancy okay that covers your trip dance so what is the big big thing that i want you guys to remember as adverse effects it's really this heart stuff you really want to be careful in people who have underlying coronary artery disease prince metals angina they have unstable angina they have peripheral artery disease they have high blood pressure because it's going to clamp down on things paresthesia is called extremities but also a big thing contraindicated in pregnancy all right ergots ergots are kind of your second line okay so after you've tried giving a tryptin it didn't work you may try giving an ergot and again ergots are like your dihydrogotomy guess what it does almost all the same stuff we just talked about so this would be a nice quick review it causes that vasoconstriction effect and if it causes that vasoconstriction what will that do that can lead to angina of the actual coronary vessels this could lead to prinz metals or worsen if they have prince metals and this could even lead to an acute myocardial infarction very rare though it could also act on the peripheral vessel and lead to increased blood pressure and it can also cause clamping down of those peripheral arteries worsening already present peripheral artery disease so avoid in patients who have have coronary artery disease they have prinz metals angina they have high blood pressure or they have peripheral artery disease the next thing remember i told you that whenever you give these drugs they act on very particular types of receptors that are present on the chemo triggers and you see this area here it's in the medulla it's called the chemo trigger zone it's near the area postrima okay whenever someone has is taking these ergots they like to stimulate and activate the five h ht3 receptors present on the chemo trigger zone remember i told you that they stimulate all 5 hd receptors if you do that the chemo trigger zone will activate the the medic center and trigger nausea and vomiting okay so that's another thing to be thinking about it also induces contraction of the smooth muscle of the uterus so if you induce smooth muscle uterine contractions if you've got a baby in there and you try to pop that sucker out too early not a great idea so it's contraindicated in pregnancy it's kind of starting to sound the same right yeah that's good all right what else all right so then another thing that ergots can do is they can also act on the liver and really jack up that liver a little bit and increase your liver function enzymes right so your lft so it increases your ast your alt your outflow stuff like that and so it does have this hepatotoxic effect if you will right so think about checking lfts on these patients whenever you put them on them okay especially if they're using it frequently the other thing is that it can again act on the nerve similar to the triptans and cause some paresthesias so you may get some again some numbness some tingling sensations of the lower extremities and then it can also induce weakness as well with prolonged use all right the next thing i want you guys to be thinking about very important to take away from this migraine kind of medication pharmacology video is that whenever someone is taking let's say they take tryptanes and then they also take on top of that ergots or they take tryptans but they also take an ssri or a tricyclic those are things to be thinking about so again what i want you to remember is serotonin syndrome can happen whenever someone is taking let's say for example a tryptan and maybe one of the following drugs maybe they're taking an ergot with that and they're taking too much of it or they're taking an ssri or they're taking a tricyclic antidepressant right things like that if they're taking something that uh besides something that's naturally this increases serotonin and you give other things that either increase serotonin as well there's a risk of serotonin syndrome it's a straightforward concept right so what i want you guys to remember is that whenever someone's taking a tryptan they're adding on an ergot or they're taking an ssri or a tca with that basically it increases their serotonin concentration and makes everything really hyper excitable and so how will this kind of present well they can present really like agitated okay so they can have what's called psychomotor agitation and they can also present with a lot of delirium okay so kind of an altered mental status if you will the other thing is it really increases your sympathetic nervous system type of activity so your sympathetic nervous system is going to be hyperactive and that's particularly really going to affect the heart and when it acts on the heart it just acts as a you know a positive inotrope positive chronotrope so it's going to increase your blood pressure and it's going to increase your heart rate also you're going to activate the hypothalamus what does your hypothalamus do hypothalamus will activate the sympathetic nervous system and increase or reset your body's temperature so it's going to increase your body temperature also what does your sympathetic nervous system do it stimulates sweat glands and so you're also going to have increased sweat production so there's going to be increased sweating or diaphoresis so you're going to have tachycardia hypertension hyperthermia or pyrexia as well as sweating along with agitation and delirium now here's the next thing we have the autonomic symptoms we have the psychiatric symptoms now the next thing is you're also going to have certain types of somatic symptoms so somatic symptoms that you can develop is that whenever you have increased amounts of serotonin you know these things called muscle spindles remember these little guys we've talked about them before they're called the muscle spindles whenever you have increased 5-hydroxytryptamine serotonin it stimulates the living beeswax out of these muscle spindles and they start hyper firing and when they hyper fire and send all that information you know whenever muscle spindles are hyper firing they're sending information to your spinal cord and then from there coming back it activates your motor fibers right you have your alpha motor neurons your gamma motor neurons all that stuff but basically if you increase the activity of your muscle spindles and you have them over fire it's going to cause the muscles to become really hypertonic and so if you cause that that hypertonia so let's say what's the first thing it's going to increase your tone and also if you go and tap on their patellar tendon or you try to elicit a reflex that's going to be really hyperreflexia so they'll have increased deep tendon reflexes even with the risk of clonus okay the other thing is remember what i tell you when they have lots of serotonin serotonin loves to act on 5-ht receptors that are present on the chemo trigger zone what is that going to induce nausea and vomiting that's going to induce nausea and vomiting also if you guys watched our videos on gastrointestinal physiology like the enteric nervous system you will know that 5-hydroxytryptamine or serotonin loves to stimulate the motility of the gi tract so if you have someone with serotonin syndrome and they have increasing amounts of serotonin what is that going to do to the motility of the gi tract it's going to increase it you're going to be peeing out your butthole so it's going to induce diarrhea that's serotonin syndrome so when we see serotonin syndrome it is a very important thing that we need to diagnose and we need to treat them effectively okay ergot toxicity so this is not as common as it used to be you may see this on your board exams but ergot toxicity is usually whenever someone is either overdosing on ergots right they're taking too much dihydro or gotome it used to be back in the day you were taking something like this as well as there were certain plants like rye bread that could be kind of a containing fungi particularly that had these ergot alkaloids that increase toxicity i digress but the whole point is that ergot toxicity is there is an increase in these ergot alkaloids like dihydroegotomy the two particular signs is that the patient's brain will present on fire they will kind of have these intense convulsive seizures and gangrenous necrosis because it clamps down on those vessels so hard you almost get no blood flow to the digits and so you can also get gangrenous necrosis particularly of the digits so this is another one that you got to be thinking about sometimes they may ask you the treatment of this one and so the treatment of this is generally you're going to give anticoagulants so anticoagulants will put anti-coags you may have to give what's called low molecular weight dextran and the third thing is you may have to give vasodilators to compensate for all of that vasoconstriction okay all right the last one is cgrp antagonist now thankfully thankfully these don't have tons of side effects really it's just like pain at the injection site so whenever you inject this one it can just cause pain the only thing that you need to remember is that this is a monoclonal antibody and this does have the potential of interacting with our immune system and leading to an anaphylactic type of reaction so you do need to be kind of on guard for anaphylaxis okay so that covers our discussion on migraine medications all right ninja nerds in this video we talk about the pharmacology of migraine medications i hope it made sense i hope that you guys enjoyed it alright ninjas as always until next time [Music] you

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Length: 41min 14sec (2474 seconds)

Published: Tue Aug 03 2021