Types of Headaches | Primary vs. Secondary | Migraine, Cluster, Tension Headaches

what's up ninja nerds in this video we're going to be talking about headaches what i want to say before we get started on this video is if you guys enjoyed this video it helps you please the most important and the best way that you guys can support us is by subscribing hitting that like button and commenting down in the comment section so please do that because it helps us and enables us to keep making free videos to help people all across the world so let's talk about headaches and let's get into it all right ninja so when we talk about headaches it's really actually important for us to have like a basic definition of what a headache is right so obviously it's pain within the head but what's the cause of that pain the simplest way of defining it is you know you have these like blood vessels that run in a couple different areas like three particular areas one is these blood vessels can run in the dura mater they can run near a particular cranial nerve like cranial nerve five or they can run near blood vessels in the muscles of the head and the neck region whenever you have irritation stimulation agitation of these vessels that are near what three structures near the dura mater so we'll put dura mater cranial nerve five which is the trigeminal nerve this is the most common cranial nerve or the muscles of what area the head and neck any time there is irritation agitation stimulation of the blood vessels of those three structures this can trigger a headache now when we talk about headaches it's also so important that we subdivide them into two types one is a primary headache which is the ones that we'll spend a good amount of time talking about later like cluster headaches migraines tension headaches or the ominous life-threatening sight threatening scary secondary headaches so you guys are probably like well how how do i pick up a secondary headache that's where you got your snoop dog coming in to help you snoop right so the snoop mnemonic which we're going to be talking about helps us to remember the red flag signs that point towards a secondary headache which can be life threatening or sight threatening so what does the snoop mnemonic tell us well you can remember s the first part of this is for systemic symptoms what the heck does systemic symptoms mean so this means you have fever weight loss myalgias what does my algae has muscle pain maybe arthralgia some joint pain things like that add on to that a other kind of double part to the s i like to add on a second one just because it helps to aid with the systemic symptoms so they have systemic symptoms like fever weight loss my algae is arthralgias and they also have secondary we'll add on here for the other s here secondary risk factors what the heck does that mean secondary risk factors so secondary risk factors include things like hiv include things like malignancy include immunosuppression so add that on there so add in kind of hiv malignancy of some kind and immunosuppression systemic symptoms think about fever think about weight loss think about myalgia as arthralgias n stands for neurological deficits what the heck does that mean that means if you have weakness on one side you have sensory loss on one side you have aphasia or speech impairment you have vision loss you're seizing those are neurological symptoms or deficits potentially oh it's for old now don't forgive me for those of you who may be greater than this age range i'm not calling you old it's you know the definition of it's greater than or equal to 40 years i'm sorry 50 years of age so old 50 years of age okay or greater now that may sound not old to some people believe me i'm 31 but i feel like an 82 year old with my body nowadays but we got systemic symptoms secondary risk factors neurological deficits old greater than or equal to 50. the next o is for the onset of the headache is extremely abrupt or acute and this is where you want to think about something so if someone has just an acute or abrupt onset of a really intense headache think about this term thunderclap headache which it comes on acutely and intensely that could be a sign of something very ominous like a subarachnoid so again we got systemic symptoms secondary risk factors neurological deficits old greater than or equal to 50 onset of a headache is abrupt and acute the next p is if they have any papilla edema so whenever someone has papilla edema they have high intracranial pressure it presses on the optic nerve and swells up around those optic discs you can pick that up when you look inside of their eyes and you see some kind of loss of the disk margin there okay so you can see that on fundoscopic exams the next p in this snoop mnemonic is it's positional so the headache is positional and so commonly we say it's worse when you're lying down and then better sitting up this may sound like not very scary but this can be an ominous sign of potentially like a brain tumor okay so we got systemic symptoms secondary risk factors neuro deficits all greater than or equal to 50 onset of headache is acute or abrupt papilloedema and positional headaches the next one is if there is a pattern change so is there a pattern change of the headache what does that mean let's say that your headache is usually you have a very common type of headache symptom it's dull it's achy all of a sudden it's this stabbing pain this throbbing pain this thunderclap type of pain it's the worst headache of your life you've had headaches before but it's not the same it's different that could be an ominous sign or a red flag sign and the last one of the red flag signs is that it can be the headaches can be precipitated by a maneuver called the valsalva maneuver what the heck you know whatever you're trying to bear down you know drop a deuce you you start causing that kind of valsava maneuver now what valzaba's maneuver does is it increases kind of your intra-abdominal pressure you're into thoracic pressure and you know veins that are draining from the brain you have your cerebral veins they'll drain from the the internal jugular vein and then into the superior vena cava which is in the thorax if someone has a valsava what that does is that'll actually decrease the venous drainage coming from the brain and if you decrease the venous drainage that venous blood will actually kind of congest into the brain area and increase the intracranial pressure what if somebody already has a condition where they have increased intracranial pressure they valzava they bear down or they cough a lot you increase their intrathoracic pressure you decrease their venous drainage and increase their icp even more that's also going to worsen their headache or potentially precipitate a headache so we nailed down our red flag signs so now that we know what are the things that would queue us up to say okay this is not one of the migraine this isn't a cluster this is an attention headache this is scary this could be a secondary headache that i got to figure out what are those types of secondary headaches i like to break them down into three different categories okay it's either a mass occupying lesion so if you have a mass occupying lesion it's due to the accumulation of one of three things that are within the skull according to the monterey kelly doctrine there is either an increase in blood an increase in csf or an increase in brain tissue whether that be normal brain tissue abnormal brain tissue whatever there's an increase in one of those three things so let's first talk about an increase in blood what could be reasons why you would have an increase in blood and that could be causing these secondary headaches well if you had some kind of underlying history let's say that the person came in and said ah i have a headache and then whenever you kind of talked with them there was a history of trauma well that should make you think what if they have like a bleed like an epidural hematoma a subdural hematoma or an intracerebral or intraparenchymal hematoma so these are things that you should think about do they have a epidural hematoma do they have a subdural hematoma do they have a intraparenchym hematoma the other thing to think about is what if the patient also has hypertension intraparenchymal hematomas don't always have to be by trauma they can also be by things like hypertension or aneurysms coagulopathy things like that okay the next thing that you want to think about if someone has trauma history think about these but if someone also comes in with this classic sign this is this is honestly if you ever hear this or it's on your vignette a clinical vignette they come in and they say i have a or it's you see it this headache describes as a thunderclap headache or you see it described as the worst headache of my life this is kind of a telltale sign of a subarachnoid hemorrhage so what do you want to be thinking about blood within that subarachnoid space like a subarachnoid hemorrhage what are other signs that may clue you into thinking about a subarachnoid hemorrhage not only this kind of descriptor within the clinical vignette but also think about do they have also meningeal signs what are some meningeal signs do they have nausea do they have vomiting do they have some photophobia do they have phonophobia right so sensitivity to light sensitivity to sounds do they have any neck stiffness or nuclear rigidity could all be signs of someone having potential like a subarachnoid hemorrhage or do they have neurodeficits as well so is there any kind of weakness potentially these are all things to think about when someone presents with a subarachnoid hemorrhage or a headache that you suspect is a subarachnoid hemorrhage okay so we got the blood ones right so again three types of things within the mass occupying lesion increase in blood what how could we remember trauma subdural epidural intraprincipal but remember intraprinciple can also have other causes thunderclap headache worse headache of the life with meningeal symptoms and neurodeficits think about subarachnoid hemorrhage what's the other one there's an increase in brain tissue okay whether this be normal brain tissue or abnormal brain tissue there's just an increase in it what if there's a tumor and it's sitting on that pituitary gland you got a pituitary tumor here what's the most first off what's the most common type of pituitary tumor this is usually what's called a pituitary adenoma a pituitary adenoma this is by far one of the most common types of pituitary tumors now a pituitary tumors not only will you get a headache but are other telltale signs that will say oh this could be a pituitary tumor well you know it actually compresses a particular nerve what's the nerve that actually runs from the eyeballs and then crosses over right up below the pituitary gland and then goes to the the lateral geniculate nucleus what is those things optic chiasma if the pituitary gland sits on the optic chiasma where those medial fibers are running where do the medial fibers pick up visual fields from so here's the medial part of the retina where the medial fibers will come from they pick up visual fields from this area coming from my temples and it's on both sides so if the patient also presents with bi temporal hemianopia with a headache that could also be a sign of a pituitary adenoma what else what if they also present with signs of hyproprolactinemia because what is the most common type of pituitary tumor prolactinomas so if they were to have a pro a pituitary adenoma the type that would be most common is a prolactinoma so they would produce lots of prolactin they got milk coming from the nips they got gynecomastia they got decreased libido these are all potential signs so if again if there is any kind of galactoria if there is any kind of gynecomastia or if there's any kind of menstrual irregularities we'll put abnormalities and sometimes we even say decrease libido or erectile dysfunction okay so these are things to be thinking about okay what's another thing where there could be kind of an increase in brain tissue so we got pituitary tumor what if we have a big old whopping pus pocket there a brain abscess ew so if you have a brain abscess that also can cause a headache for shore skis so if there's a brain abscess and there's a pocket of pus or maybe that's a bacterial infection or some kind of infection in general these patients will present classically not only with headache so they'll have that kind of this classic triad of headache plus or minus a fever so sometimes they can have a fever and they also have particular neuro deficits and it's depending upon which area it's compressing like if the abscess is compressing on the visual area like the occipital lobe you'll develop visual abnormalities if it's compressing on the primary motor cortex you'll develop weakness on one side so it just depends upon which area that abscess is compressing so again that would cover that one so we got brain abscess we got pituitary adenoma what's another thing that can increase brain tissue the other one that you want to be thinking about here is if someone has a brain tumor like an actual like brain tumor not pituitary type so they have a brain tumor now a brain tumor there's so many different types right so you can have like glioblastoma multiforme you can have meningiomas you can even have it as a metastatic type so it came from some other area like the lungs or it came from the breast and then it spread to that area either way when someone has a brain tumor how will these headaches present remember what i said before with the signs the headache is positional so what does that mean that means it's worse when they're lying down or when they're getting up in the morning and it's better when they're sitting up okay that could be a sign the other sign is that usually these people especially if the tumors are near the upper part of the cerebrum near the cortex they have high high risk of seizures okay so these are potential things to think about here but also what else could you think about systemic symptoms do they have a low grade fever do they have weight loss oh that could be a potential thing to think about as well okay the last one we're going to talk about but we're only going to talk about it briefly because usually this last one where there's an increase in csf is actually kind of a bunch of different things within each other but we talked about blood ich subdural epidural subarachnoid brain pituitary adenoma brain tumor brain abscess if there is an increase in csf this cause here is usually due to two things and this is called hydrocephalus now but there is two different types of hydrocephalus we're not going to go into detail on this i'll just mention them there's what's called obstructive hydrocephalus and then there's another one which is called communicating hydrocephalus but either way what happens is there's this big dilation of the ventricles and so whenever you have more fluid inside of your ventricles what is that going to do well that's increasing one of the three things with inside of the skull and that's going to increase your intracranial pressure and that's a mass occupying lesions so if someone has blood within the ventricles that are plugging up the ventricles that can cause an obstruction if there's a tumor that's maybe compressing on the ventricles that could decrease the drainage if there's meningitis where the cerebral spinal fluid is supposed to drain out of the subarachnoid space and it's inflamed that can cause a communicating hydrocephalus but either way whenever there's hydrocephalus there's an increase in that csf and usually these patients can present with headache and they can also present with decreasing level of consciousness okay usually hydrocephalus will commonly present with an altered mental status decreasing level of consciousness and if you get an actual image of their head you'll see big old dilated ventricles okay but again the type of hydrocephalus could be caused by multiple different things which we're not going to talk about in this lecture okay that covers the mass occupying lesions let's talk about things that are non-mass occupying lesions but still cns pathology all right so again think about we already talked about mass occupying lesions blood brain csf one of those threes are increasing the other thing is you can have cns pathology where there's not actually a mass occupying lesion but there's something wrong with the brain or the brain tissue in some way shape or form it's just there's no big mass there so what could these things be well think about any irritation of the meninges or the actual brain tissue itself if there's irritation inflammation infection of them so sometimes if someone has what's called meningitis which is inflammation so meningitis or encephalitis so meningitis is inflammation of the meninges encephalitis is inflammation of the brain tissue so for example if i'm talking about this that's the meninges right we're inflaming those whether they're infected for some reason or they're inflamed for some reason and then if i'm actually causing inflammation of the brain tissue that's encephalitis whether that be infectious or autoimmune in some nature there's inflammation there meningitis and encephalitis again they present with the headache but they also present with fever and they'll present with those meningeal signs do you guys remember what those meningeal signs are they'll present with photophobia phonophobia they can present with neck stiffness what else could they have the positive kernigs brzezinski signs and they can also present with kind of an altered mental status a little bit confused you know especially if they have encephalitis viral encephalitis you know this cause personality or behavioral changes and also they can have neuro deficits depending upon the location where that meningitis or encephalitis is if it's compressing on the temporal lobe they may have behavioral activities or if it's compressing on the motor cortex they may have weakness on one side of the body so again it depends upon the area where that meningitis or encephalitis is located okay but that kind of qq clues you in here with meningitis or encephalitis the next one here is if you have a very interesting condition which to be honest with you it can kind of fit within both cns pathology of this non-mass occupying and actually kind of can be within the category of mass occupying a little bit and i'll explain why this next condition here is called cerebral venous sinus thrombosis commonly abbreviated cvst cerebral venous sinus thrombosis is usually due to some type of clot or blockage within the cerebral veins you guys remember all your cerebral veins right your superior sagittal sinus your inferior sagittal sinus your straight sinus your sigmoid transverse all of those things which eventually drain into the internal jugular vein right well if somebody has a clot that blocks up or occludes the actual drainage from those veins what that can do is that can increase intracranial pressure right so not only will these patients present with headaches but they'll also present with signs of increased intracranial pressure and so high icp can present with like nausea and vomiting because you compress the chemo trigger zone it can present with papilla edema because you compress the optic nerve right it can present with decreasing level of consciousness because you compress the reticular formation and we can keep on going and going and going the other thing that can happen here is because these clots usually kind of occur near the cortex there's also a very high incidence of seizures so what are some other things that can clue into cerebral venous sinus thrombosis again not only do they have this headache they have the increased icp increased risk of seizures but if you have a female so a female patient who is has anything that makes them hyper coagulable that is going to be a problematic thing and so you should think about this are they on oral contraceptives do they have factor 5 leiden do they have anti-phospholipid syndrome are they pregnant these are all things that can increase the hypercoagulable state and increase the risk of forming clots basically cerebral venous sinus thrombosis is just the dvt of the brain in in the most essential way okay so these are things to cue you into that the next thing that you want to think about is a very interesting one so sometimes if someone has a history of trauma and they actually have trauma sometimes to wear to the head or neck region they can actually dissect a couple different vessels such as the vertebrals or the carotids when you dissect these vessels okay and they can kind of look like aneurysm pseudo-aneurysms basically so again what are these called here this could be a carotid or vertebral artery dissection okay so carotid or vertebral artery dissection usually secondary to some type of trauma so again you want to think about was there any history of trauma okay that's the first thing we think about with these the second thing you want to think about with these is you know what actually like nerve fibers run up through this area between kind of these structures here what kind of nerve fiber runs up through here and goes and supplies parts of like your eyeball and also some of the sweat glands your sympathetic plexus so sometimes what can happen is from that dissection it can compress on the sympathetic plexus if you compress the sympathetic plexus and you end up with ptosis meiosis anhydrosis what is that called horner's syndrome so sometimes if someone has trauma and they also present with horner syndrome and on top of that neck pain and one more thing tinnitus which is usually pulsatile this should clue you into doing more investigation to thinking about a carotid vertebral artery dissection okay all right boom shabam let's move on to the next one the next one that i want you to think about is a very very interesting kind of condition this condition has a very interesting name as well it's a son of a gun it's called idiopathic intracranial hypertension also known as pseudo tumor cerebri so in this condition the patient naturally has elevated intracranial pressure okay so their characteristics is they will have a headache they will have constantly elevated intracranial pressure which will present with what kind of signs nausea vomiting papilla edema decreased level of consciousness what else so let's see if you guys remember nausea vomiting from compression of the chemo trigger papilla edema from compression of the optic nerve decreased level of consciousness from compression of the reticular formation and last but not least they can also compress cranial nerve six which can lead to diploplea okay the thing to think about is not only will they have headaches not only will they have high icp but do you remember what was one of the other p's within the snoop mnemonic wherever someone was valsaving or they were coughing like intensely and it caused that shoot up in high intracranial pressure and if somebody already has elevated intracranial pressure it can worsen it and make even the headache more intense guess what kind of headache this would be triggered by this headache would be worsened by it could be precipitated by a valsalva so we would say this one is precipitated you see isn't it awesome when sometimes things just come together precipitated by a valsalla maneuver now here's the thing that's really interesting about this you would think what is the reason for this hydrocranial pressure we don't really know what we know is this is common in females who are obese and on oral contraceptives that's one of the things and sometimes even tetracyclines is another weird one so if you see an obese woman who is on oral contraceptive tetracycline she has headaches she has nausea vomiting papillaedema she has decreasing level of consciousness she also has diploplia and then you also see that her headache is worse than by villa valzava's maneuver and then you also get imaging and all the imaging is normal that should make you think about what pseudotumor cerebral idiopathic intracranial hypertension well how do i diagnose this i think this is a good this is one of the few that i want you guys to think about diagnosis diagnosis for this is you obtain an lp a lumbar puncture and that produces this insanely high opening pressure because of all the elevated intracranial pressure they have but their ct and all the labs that you run on their lp will be normal there won't be any signs of infection or inflammation or anything like that it'll just be they have this idiopathic intracranial hypertension okay that covers the cns mythology that is non-mass occupying let's go over the things that are cns pathology but it's actually from external causes so the last part here which is again there's going to be some type of like external cns pathology basically there's nothing wrong with really the brain intrinsically it's something else outside of the central nervous system that is inducing these headaches so what could that be well you know whenever somebody has a you know good old sinus infection they got some infection of their sinuses inflammation of the sinuses this can definitely cause a headache so if you think someone has like sinusitis what would be a way that would clue you to saying okay this is definitely not a primary headache and how would i know that it's one of these many different types of secondary headaches it's easy right so they got a headache they also have maybe a low-grade fever they also have a rhinorrhea but this rhinorrhea is probably purulent they may even have some nasal congestion from all of that good stuff that's in there what else they can have tenderness to palpation of their sinuses so you go ahead and just boop and they're like oh that could be a potential sign of sinusitis right so that's kind of a kind of an easy one to think about the next one is very interesting so let's say that you have a patient comes in they're complaining of these headaches and you look at their eyeballs and their eyes are really kind of like irritated and red so this one you see so far i want you to think about acute angle closure glaucoma so acute angle closure glaucoma will definitely present with a headache so orbital pain right like they'll be headache around the orbital area they also will present with ocular hyperemia they'll present with a mid and fixed dilated pupil okay and so also maybe some decreased vision all of these things should kind of point towards an acute angle closure glaucoma so if they have a headache they also have ocular hyperemia they have a mid fix dilated pupil and on top of that they have decreased vision this should make you think of that type of condition all right the next one here very cool one is actually called giant cell arteritis or temporal arteritis so if someone has what's called giant cell arteritis also known as temporal arteritis so with this one you definitely present with a headache but it's usually over the temporal region thus the name temporal arteritis it's usually due to the inflammation or vasculitis of that vessel the superficial temporal artery what happens is you know what's interesting another thing that you can see on the the vignettes is that someone will say oh man i have this pain in this area of my temple it's causing a headache but it's so tender that even when i brush my hair it's so painful that's kind of a telltale sign on the exams the other thing to think about is if they have any claudications what does that mean they have kind of like pain or they have kind of like they get really fatigued within the muscles of their chewing muscles the mastication muscles because that blood coming from that area the external carotid artery can also kind of get a little vasculitic that supplies the temporal artery and if that gets vascular it can affect the blood flow to the mastication muscles and they can get fatigued or tired or painful during chewing so this is called jaw claudication the other thing is the vasculitis can extend into what's called the ophthalmic artery and this can even lead to visual changes so potentially visual changes sometimes with the worst case scenario if not corrected very very quickly can lead to blindness and one last thing to think about here is that it's commonly associated with a very particular condition called polymyalgia rheumatica polymyology rheumatic is when you have this kind of like muscle tenderness and pain of like the proximal upper extremities and the proximal lower extremities very very commonly associated i think this is a good thing to talk about diagnosis though how do you diagnose this condition you need to you can actually check an esr and a crp and they're often elevated because of the inflammation but the gold standard is what's called a temporal artery biopsy so i think this is one of those types of tests that you'll definitely want to remember for your exam okay all right the last type of secondary headache that is kind of an external one that i want you guys to think about very very important one to remember here is going to be trigeminal neuralgia this is a very very sad type of problem here so trigeminal neuralgia so trigeminal neuralgia is actually whenever somebody has a headache okay it's a unilateral headache and it's very particularly described it's usually in a in particular distribution like v2 v3 division of the trigeminal nerve and what happens is when these people have these headaches it's usually described as stabbing or electric or like lightning or lancinating type of pain it's this intense unilateral pain that is lancinating stabbing it's electric it's lightening pain that's usually within that type of unilateral distribution of v2 and v3 okay the other thing is that if you get imaging on these individuals or you do other parts of their other parts of their neural exam is relatively normal they really don't have any deficits on their neural exam but another thing is that this pain is exacerbated by very simple things like touch or even something as simple as like chewing or wind blowing across their face and this can happen so many times this can happen up to 10 to maybe even 100 times a day and so this is also called you know the tick doula rule where they actually have like kind of this very high risk of suicide from this condition because it's happened so painfully and so frequently sometimes and so what you'd have to do is for this condition they would have a normal neural exam but the diagnosis i think this is actually an important one to think about here is that you'd have to get kind of an mri or an mra and it would show compression of the trigeminal nerve okay of cranial nerve five by a very particular vessel by the superior cerebellar artery so that's another big thing to remember for your exams when you think about trigeminal neuralgia unilateral headaches stabbing electric lancinating lightning type of pain worse whenever someone touches it they're chewing wind blows across it can happen 100 times a day potentially and you need to really get an mri mra and usually what that's going to show is the superior cerebral artery is going to be smashing or compressing on that trigeminal nerve okay that covers our secondary headaches now let's take our time and go through the primary headaches all right ninjas now that we've finished secondary headaches let's talk about primary headaches and there's three particular types that i need you guys to remember migraine it is the second most common type of primary headache cluster headaches is the less common or the least common type of primary headache and then the last one here is tension type headaches which is the most common type of primary headaches so when we talk about these what i want us to cover systematically here is what are their causes how do those particular causes lead to the actual clinical features that we see via the pathophysiology how do we diagnose it and then how do we treat them all right so if we go systematically here let's start with migraines and talk about the causes or triggers if you will because there's really no true defined cause behind migraine there's maybe some genetics that are involved here potentially that there may be some calcium channeled like dysregulation or abnormality where the calcium channels may be a little bit more hyperactive for some reason but really the only gene that's really been chased back to migraines is if someone has what's called a familial hemiplegic migraine there can be genes traced back to that but primarily the most common triggers if you will for migraines is usually red wine chocolate cheese oral contraceptives and you can't go wrong by always saying stress so any kind of stress of any kind really can cause migraines all right so we have these particular factors or triggers how do these things lead to migraines like what's the pathophys behind it to really kind of briefly go over and the only reason why we're not going to go crazy on it is just because it's not truly well known what the thought is is that there is something that triggers the beginning of this in some cases called a cortical spreading depression theory so what what the heck does that mean so cortical spreading depression theory in the most basic sense means there's a particular area of the brain that becomes hyper-excitable and starts firing and then leads to this firing that spreads throughout the actual cerebral cortex and basically the whole thought behind this is that whenever there's this spreading of depolarization it can lead to these things called auras and auras are usually symptoms that present before an actual migraine like headache actually starts what's the most common type of aura that you guys can think about if you've ever had a migraine you know it you get like these fuzzy white spots or different kind of like shimmering things that would show up within your eyes right they're called scotomas and so the most common type of aura is usually going to be these things called scotomas or visual basically abnormalities that present before you actually develop a headache but that's the theory is that these this cortical spreading depression theory occurs in a particular area of the brain and that spreads throughout the rest of it what happens though is that during this spread there's activation of particular pain receptors okay noisy acceptors of cranial nerve five and this can trigger the release of a couple different types of substances and these include vasoactive peptide so we'll put vp cgrp which is referred to as calcitonin gene regulating peptide and then what's called substance p and basically there's three particular things these these guys do one is they stimulate mast cells you know what mast cells like to do they like to release inflammatory mediators things like histamines and they also like to release other inflammatory mediators like prostaglandins okay and you know what these guys do they induce inflammation right they're going to cause vasodilation increase capillary permeability all that good stuff well guess what these chemicals vasoactive peptides cgrp and substance p also do they also act on the blood vessels and they cause the blood vessels to undergo what's called vasodilating so they dilate and also it can cause them to become more permeable as well so not only is there vasodilation but you can also make them a little bit more leaky where things leak out of it like plasma proteins in some shape or form right so either way all of this stuff all of these chemicals that are either causing mast cells to induce inflammation or these chemicals directly causing inflammation lead to the activation of other nearby pain receptors in the vicinity of where that neurogenic inflammation is occurring and guess what the most common type of noisy acceptor is it's the noise receptor connected to cranial nerve five so usually cranial nerve five has pain receptors that pick up these actual neurogenic inflammation near these blood vessels and where is all of this usually most commonly occurring it's usually occurring in the meninges this is usually most common in the meninges where all of this kind of reaction is taking place when they get activated these trigeminal nerve it sends these afferent signals into the trigeminal nucleus from the trigeminal nucleus it'll send this up to the thalamus and then from the thalamus this will send this information the sensory information to the cerebral cortex like your sensory cortex and what will the sensory cortex perceive pain where does the trigeminal nerve actually pick up sensations from the head so if you have pain coming from the head what you may feel headaches so that's kind of the whole theory behind this pathophysiological mechanism there's one other mechanism and it's important to remember this one just because of when we talk about migraine medications and their mechanism of action one of the other things that has been seen with migraines is that there tends to be lower levels of 5-hydroxytryptamine also known as serotonin when there's low levels of serotonin it tends to induce a lot of vasodilation increased capillary permeability leads to this neurogenic inflammation and activate this pain pathway so that's another thing to think about is that there's lower serotonin levels as another potential trigger for this pathway all right boom roasted we knock out the pathophys and triggers our etiology of migraines what about for cluster headaches alright so for cluster headaches when we talk about this type of headache and again it's etiology the triggers it's believed to be primarily and predominantly due to smoking so tobacco smoke and stop puffing the you know the chiba or it could be due to red wine when or it could be due to you being a male right so these are just common triggers but also you can't go wrong by saying any kind of increase in stress so either way some of these triggers they lead to the activation of a particular area of the brain that just seems to be dysfunctional for some reason in these patients which is the hypothalamus so the good old hypothalamus done did us wrong in cluster headaches so what does that hypothalamus do it becomes activated and when it becomes activated by these particular triggers it sends signals down to your parasympathetic nervous system stimulates kind of the parasympathetic fibers that go to what's called the sphenopalatine ganglion activates these parasympathetic fibers and these parasympathetic fibers go to particular areas which includes the glands like the lacrimal glands and the nasal glands and so what happens is if you stimulate these lacrimal glands it'll obviously lead to lacrimation and if you stimulate the nasal glands it'll lead to this nasal secretions very important to remember these especially when we get the clinical features all right and so the other thing that will happen here is that you can also have some release of these again the parasympathetic stimulation of small little blood vessels and what will happen is these little blood vessels will undergo some vasodilation and this can cause two things remember vasodilation in migraines cause a lot of neurogenic inflammation that's one thing it's going to lead to neurogenic inflammation but the other thing is it causes a lot of increased blood flow near the conjunctiva so it causes conjunctival hyperemia the other thing which we already said is it leads to a lot of neuro genic inflammation what's the problem with that neurogenic inflammation the problem with the neurogenic inflammation is that this is going to cause inflammation of blood vessels guess what nearby particular cranial nerves which includes just happens to be cranial nerve five if you activate these noisy acceptors they will send that information into your trigeminal nucleus the trigeminal nucleus will then send that information upwards to the thalamus and then from the thalamus it's going to send that information or sensory signals to your sensory cortex your cerebral cortex and what was this problem neurogenic inflammation it activated noisy acceptors noise receptors are for pain where's the trigeminal nerve pick up sensations from the head if you have pain coming from the head what's that called a headache so that's where you get the headache aspect of it now the other thing that's really interesting is that this neurogenic inflammation all can also can occur near this blue structure here called the cavernous sinus and it can cause the cavernous sinus walls to become inflamed so you can actually call it you can inflame the cavernous sinus and this is what's really cool there's a sympathetic plexus that runs through the cavernous sinus that goes and supplies the eyeball and if this cavernous sinus is inflamed it's going to put pressure on these sympathetic fibers and if you put pressure on those sympathetic fibers these sympathetic fibers go to the pupil muscles and cause them naturally to dilate but if you can't because you're compressing them this will cause meiosis it also goes to the muscles of the tarsal plate and causes them to elevate the eyelid if you can't do that they will droop and it causes ptosis but here's the thing there is no anhydrosis so it's not technically horner's syndrome it's kind of like a partial horner syndrome okay so this is the particular types of pathophysiology that we see here present in cluster headaches let's finish up down here with the easiest one thank goodness right you're like dang i'm sick of this this is tension headaches now tension headaches have particular triggers and generally this is because of like the muscles being tight or tender it could be due to dehydration it could be due to stress any kind of emotional stress or physical stress and then also you can't go wrong by saying you're sleep deprived so then when there's decreased sleep or sleep deprivation these types of triggers what they'll do is is they'll cause particular muscles like in the pericranial muscle area to become tight stiff and tender when these muscles and the pericranial area near the head the neck and the shoulders become really tight it activates tiny little blood vessels that are nearby these muscles and whenever you activate the actual blood vessels or stimulate these because of all of these triggers the blood vessels nearby these muscles guess what type of nerve fibers are present near these vessels cranial nerve five and so cranial nerve five will have afferents that will pick up this kind of noise deceptive sensation coming from the vessels near the skeletal muscles of the head the neck and the shoulders and send that information into the trigeminal nucleus in the brainstem go up to the thalamus and from the thalamus it'll relay that sensory information to the cerebral cortex which will present as pain and pain is coming from the trigeminal location which is going to present particularly in a very particular pattern of headache okay which we'll kind of talk about in a second but that's kind of the basic mechanism of tension headaches now what can happen is over time is as these headaches continue to persist as tension headaches persist your central nervous system can undergo a process called central sensitization and so you actually can have worsening headaches over time any sensation can be perceived as way more painful than usual also known as hyperalgesia but that's the basic mechanism behind tension headaches now let's talk about the most important part of the actual primary headaches being able to differentiate them based upon their clinical features all right engineers so what we're going to do now is we're going to talk about the clinical features of the following primary headaches again migraines cluster headaches and then tension type headaches so for migraines you can actually remember the clinical features here by the mnemonic pound okay pound baby all right so p this is basically if it's pulsatile in nature pulsatile sometimes i like to add in another two like photophobia and photophonophobia o is for one day in duration typically we say anywhere from like 4 to 72 hours though u is for unilateral n is for nausea and vomiting and d is it's for disabling and its intensity okay so again pound mnemonic is pulsatile i like to add in photophobia phonophobia o is for one day and duration u is for unilateral n for nausea and vomiting and then d for disabling that's kind of the easy way to remember this type of presentation now usually location wise again it's going to be unilateral near orbital retro-orbital and even a little bit more frontal area as well the other thing that you guys need to remember that is associated with migraines and we already talked about a little bit we kind of preluded into it when we talked about potentially that cortical spreading depression theory is auras so auras can also occur in patients with migraine it can either precede the migraine or you can have auras without even having a migraine so when we talk about auras there's different types and the auras are depending upon the location that's affected so for example if we said kind of the occipital lobe what would that lead to well if it was affecting the occipital lobe then you may develop certain types of visual abnormalities and visual abnormalities are going to be the most common type of aura so i really want you to remember these and these consist of scotomas so they're scintillating scotomas they're centroscotomas and then there's also other different types of just visual abnormalities like different types of zigzag lines and fortification spectra this is a really important one the other thing is what if it kind of involves like a sensory area for example what if it hits like what if the auras spread and it involves like the sensory cortex well then this can lead to sensory abnormalities and what could that sensory abnormality present as maybe it presents with parasthesias of a particular part of the body maybe the arm maybe at the leg so on and so forth what if it goes on and involves another part what if it involves like the motor cortex of some kind and it hits the motor cortex well then it can lead to a motor abnormality and maybe that motor abnormality will present as weakness on one side of the body so again that's a very interesting thing to think about what if the or is actually spread to the brain stem as well well if they hit the brainstem this can sometimes lead to what's called brain stem auras so brain stem auras also used to be called kind of basilar auras or basilar kind of migraines these generally involve particular cranial nerves so you can actually involve like diplopia which is kind of double vision you can develop vertigo from involving like the vestibular nuclei you can cause decreased hearing from involving the cochlear nuclei you can even lead to dysarthria by interrupting the activity of the glossopharyngeal nerve or the vagus nerve or even the hypoglossal nerve okay another thing here that you can also present with besides having these auras involving the brain stem or involving particular territories of the cerebral cortex sometimes it can actually involve the retina itself and this can lead to a subtype called retinal auras okay or ocular migraines sometimes they call them retinal my auras or ocular migraines there's another type of aura that i want you guys to remember because this is common in people with who and family members sometimes you can actually have what's called a hemi there's another subtype called a hemiplegic migraine and so this is the one that can kind of present with this weakness so usually they present with unilateral weakness and this can last for a couple like actually can last for up to 72 hours okay for it's up to so greater than or equal to 72 hours and so whenever you see someone who has a migraine and they're also having weakness on a particular side of the body and they may also have some sensory abnormalities like paresthesias and visual abnormalities and speech difficulty you should have a differential for that you should think about oh is this person having a stroke so that's another thing to think about sometimes migraines can actually be misdiagnosed as strokes but again you have to go through and particularly think about what is the particular cause get imaging to really verify that all right so that covers the clinical feature so what is the big thing that i want you guys to take away from clinical features i really want you to remember this mnemonic okay that's the big thing to take away from here migraines can be remembered by being pulsatile one day duration unilateral having nausea vomiting and disabling you may or may not have auras that are actually going to precede the actual headache and sometimes you can just have auras without migraines if you have an aura they can present in this particular type of fashion one that i just want you to be careful of is hemiplegic migraines they can present somewhat similar to a stroke so you have to think about that and make sure that you order the appropriate imaging to rule out that it's not a stroke and it's just a hemiplegic migraine all right so when we talk about cluster headaches what are the clinical features of cluster headaches well the big thing that you guys want to think about is it can present like location wise it's usually unilateral okay so it's on one side the next thing that you guys need to remember is that where does it usually occur in that one side usually it's orbital super orbital frontal region so again you want to remember that it can be orbital supraorbital or frontal regions of the head the next thing is how do we classify the headache the headache is actually particularly referred to as stabbing burning in quality right so it's stabbing burning sharp is another kind of description sharp in quality the next thing that you guys need to remember is duration how long do these actual types of headaches last these can last somewhat of a decent amount of time it really depends generally these can last anywhere from five minutes up to three hours but what's interesting about these is that they occur in clusters so when i say that they occur sometimes in one day you can have one to eight episodes per day and then what can happen is you can go almost 12 months without having another episode of these cluster headaches because you go into this remission type of period and then in the same size season that you develop this at the same time of the day again you'll develop these cluster headaches so they have this kind of cyclical type of pattern to them the next thing is that they also have associated symptoms that you guys want to remember and that is described by what we talked about with the parasympathetic symptoms so remember what were the autonomic nervous system types of effects that were involved here we had rhinorrhea and sometimes it can even lead to nasal congestion the rhinorrhea was from the parasympathetic nasal secretions right it can also lead to lacrimation because of the parasympathetics increasing the lacrimal gland secretions it can cause conjunctival hyperemia because it caused that vasodilation of the blood flow near the actual conjunctiva and it can even lead to a partial horner syndrome where they have meiosis they have ptosis but they do not have anhydrosis so that's how we remember that the only other thing that you want to remember is that these patients are often very restless and they don't like to stay still they like to constantly be moving so they're restless and can't stay still they're constantly moving constantly trying to get around to help to reduce this pain alright the next thing here when we talk about the last one here tension type headaches the clinical features it's important to remember that this one is the only one that is bilateral so this is going to present with that bilateral headache it also tends to be more within the frontal and temporal areas so frontal and temporal areas and when we describe the characteristics of the headaches it tends to be not throbbing or pulsating so it's usually non-pulsating in nature and but more specifically how do we describe it than if it's non-pulsating it's usually described as like a band so band-like so there's like a rubber band or a huge rubber band that's just like around their head or a vice so it's vice like imagine having like a vice grip wrapped around your head and you're just clamping down or tightening so it's non-pulsating it's band-like it's tightening it's vise-like is kind of the way that we describe it the other thing for duration is that it tends to be greater than 30 minutes but it can last up to a week but typically typically the common duration is four to six hours long okay so again when we talk about this one it's bilateral frontal temporal headaches that are non-pulsating non-throbbing usually band like vice like duration is usually greater than 30 minutes but it can go up to a week typically four to six hours the other big thing to remember for this is that there is no nausea vomiting there is no photophobia there is no phonophobia as compared to migraines which we'll present with photophobia phonophobia and potentially nausea and vomiting all right so now let's finish up with this aspect of these headaches talking about diagnosis and then treatment so again when we're talking about diagnosis we're diagnosing migraines cluster headaches and then tension type headaches now the nice thing about this is that there's no real true imaging you don't really need imaging if this person has the classical features of a migraine or a cluster headache or a tension headache these are clinical diagnoses so how do we clinically diagnose these well migraine with aura what do you think you need guys aura so you need to have some type of aura symptoms and generally these aura symptoms sometimes they'll say you need like more than two or three of them but again just to remind you this could be like those scotomas like scintillating skatomas this could be sensory symptoms this could be motor symptoms again just going off of what we were talking about over to the left right so you need to have some type of aura symptoms the other thing that you need to have is you need to have at least two or more of these migraine attacks that present with a preceding aura so greater than or equal to two attacks that present with a preceding aura okay so that would have that would be how we describe migraines with aura how we technically diagnose that condition now if it's a migraine without an aura they have a headache but they don't have that preceding viscotoma scintillating sketomas fortification spectra sensory motor any of those things before and they just have a migraine you have to have five plus attacks within a lifetime second thing is that you also have to have fulfill that pound mnemonic okay so in other words it has to be let's see if you guys remember pulsatile add in photophobia phonophobia one day in duration unilateral nausea vomiting and disabling intensity and then the last thing that you have to remember with this is that it is worse with exertion in comparison to someone who has tension type headaches which is not worse with exertion okay so that's how we diagnose meyer with aura you need aura symptoms and two plus attacks with a preceding aura migraine without aura you need five plus attacks you need to fulfill the pound mnemonic and it has to be worse with exertion all right what about cluster headaches for cluster headaches you have to have five plus attacks and those attacks have to present as a cluster headache would which is unilateral and it's usually going to present in this kind of orbital super orbital frontal fashion it's stabbing it's sharp it's burning in nature it's usually in that cyclical type of cluster pattern you also have to have one or more of the following autonomic symptoms that we talked about i'll just give you two as the example maybe that's the lacrimation or that's the rhinorrhea plus our mind is like the nasal congestion and again all the other ones so what were they to see if you guys remember rhinorrhea lacrimation conjunctival hyperemia and partial horner centered with meiosis ptosis but no anhidrosis and then the last thing that you have to remember for these is that they are super restless and agitated and have a high risk of suicidal attempts but they constantly need to be moving to feel comfortable the last one that i want you guys to remember here is tension type headaches and you need two or more of the following types of things it has to be let's do a different color since we've been saturating this blue let's do it has to be non-pulsatile or non-throbbing okay that has to be one thing the second thing is that it has to generally also present with no nausea vomiting or any kind of photo no photophobia and no phonophobia okay so it's usually that non-pulsatile it's bilateral all the characteristics that we said non-pulsatile bilateral it's tight it's vice-like it's band-like they have no nausea vomiting no photophobia no phonophobia what else the other thing is that it is not worse with exertion in comparison to migraines which are worse with exertion and last but not least is that they have this increased sensitivity to light and sound but there is no aura okay so just remember that there's no aura present here all right so now we're going to do is we're going to finish up talking about the treatment of these primary headaches right so migraine cluster and tension type headaches so with migraines one of the first things that you can do before you even start going and giving medications or doing anything is that sometimes these patients actually benefit from just putting them in a quiet room a dark room and just letting them rest because often sometimes the triggers for these individuals is stress remember what i said there was increased stress that could be bright lights that could be loud sounds there could be emotional stress they could be sleep deprived and so putting them in an area where it's a little bit calmer also what's this other symptoms of migraines they have photophobia sensitivity to bright light phone phonophobia sensitivity to loud sounds and so if we put them in a very quiet a very dark room and we just let them rest that may be the very thing that they need to get over a migraine if that doesn't work though then we can start on the abortive therapy options now when someone has a migraine and it does present with nausea or vomiting it's a great idea to replace some of that volume loss with iv fluids so giving a person a one liter bolus of normal saline 0.9 normal saline is not a bad idea okay so giving them some iv fluids the other thing is what if you want to stop them from vomiting because you want them to be able to take oral meds generally in those kinds of situations in acute situations you may give iv im sub-q intranasal but if you're trying to give oral meds maybe you try to stop their vomiting and so you can give antiemetics and so the particular types of anti-medics that are commonly given could be like metoclopramide and then the other one could be like pro-chlorazine okay so these are particular medications that you could give to stop some of the nausea so you can give them fluids and you can give them antibiotics the next thing is if you've started off kind of that nice symptomatic treatment you can start down your kind of algorithmic pathway first thing is reduce a lot of that neurogenic inflammation give them medications that reduce inflammation what are those kinds of medications nsaids so giving them some type of non-steroidal anti-inflammatory drug things like for example ibuprofen or you could even give something like naproxen now the problem with these is that these are oral what if a person's vomiting and you can't really give them the oral mess because they're just going to vomit right up sometimes giving an iv or im form called ketoralac would be a great secondary option okay so considering that in those scenarios now if the inset isn't worked the next thing you go to is a trip tan okay so the next option here is what's called a triptan so a triptan work in a very interesting way so tryptans are basically they can they act like serotonin and so remember what i told you there's low levels of serotonin and migraines if you give tryptans you're increasing the serotonin and causing these vessels to constrict and reducing a lot of that vasodilation and neurogenic inflammation and so this could be like things like sumotryptan so sumatriptane and zomatryptan and again you can give these orally there is oral dosages but generally if they're vomiting you're probably going to want to give the intranasal or the intramuscular or different types of iv injections of this the next option is if these don't work the second line after tryptans is what's called your ergot so you have your ergots or your ergot alkaloids and the most common one is dye hydro or gotamine so dihydroergodamine is pretty much just like a tryptan in a way it does help to increase your serotonin levels the only thing is is that this acts on all serotonin receptors and so not only will it cause vasoconstriction but it can also act on other serotonin receptors and maybe cause even worsening nausea so dihydro or godamine is another option so we've gone through we've gotten even given nsaids like these following ones if they can't tolerate the oral ones give them ketorlak which can be imr iv we gave them tryptanes as the first line that didn't work the second line option is ergots it's like dihydrogotamine then the next thing that you can also do you can give a drug that's been shown to decrease the recurrence of migraines and that's where a drug called dexamethasone which is a corticosteroid has been shown to be able to reduce a lot of the inflammation and also reduce recurrent rates or recurrence rates okay so we have so far within our kind of acute or abortive therapy here fluids anti-emetics nsaids for mild to moderate triptans from moderate to severe if the tryptans don't work ergots and to reduce the recurrence rate dexamethasone now if a person has a migraine okay and they continue to keep having migraines let's say that they have you know two plus migraines a week and regardless of how severe it was or they have migraines that are just crippling or disabling event preventing them from being able to carry out daily activities or they have a contraindication and we'll talk about these in our migraine medication video they have a contraindication to taking like tryptans or ergots then i should give them prophylactic therapy that prevents them from trying to develop these migraines in the future so what are those things well the first line agents there's two kind of first line agents you can pick from these whichever one you you prefer as a practitioner but generally the first one is you can give what's called a beta blocker and how these beta blockers work is they act on these beta 2 receptors that are present on the cerebral blood vessels and inhibit them and that leads to this vasoconstriction effect and so these could be drugs like propanol or metoprolol okay the other drugs that you can also consider here could be anti-convulsants now how these drugs actually work is still trying to be elucidated the thought is that these particular anticonvulsants work on different types of channels and inhibit particular like neurotransmitter release like cgrp but that's not completely known yet and what drugs are considered here this could be valproate which is an anti-epileptic and also another one or anticonvulsant called topiramate okay so these are the options that you can consider here now if these first line agents don't work for the prophylactic therapy the next one is your second line agents and this is where you get into drugs which are called tricyclic antidepressants so here we'll put antidepressant but the most commonly utilized one is a second line agent and prophylaxis is tricyclic antidepressants and this includes a drug called ami tryptolene okay now if someone has chronic migraines and you've kind of tried these things and they don't really work there's two other options one of these drugs has been found to inhibit cgrp and its effect on causing all that neurogenic inflammation so if i inhibit the cgrp i can give drugs that literally antagonize or block them and so we call them c g r p antagonists and these suckers have some intense names like gaukanizumab a renumab i think i can actually spell that one a rin umab but you want to remember the mab at the end that's the easy way to identify those okay and these have actually these are injections and they've actually been shown to be relatively effective the last thing that you could also consider here is injections where you give an injection of a botulinum toxin type a and it's been shown to inhibit the actual pain signals that are picked up from the trigeminal nerve and migraines and so giving what's called the botox a injections once every 12 weeks have been shown to be relatively effective as well and chronic migraine treatment okay so that covers the treatment of migraines both acute or abortive as well as prophylactic now what about someone who has a cluster headache these ones are very interesting it took me forever to try to figure out how this one works but when someone has a cluster headache the first line treatment that you should employ in this situation is you need to try to give them oxygen and so when we give them oxygen okay how do we do it the preferred treatment is to put them on what's called a non-re breather mask and give them anywhere from six to 12 liters per minute now what the thought is is that oxygen in these high concentrations will actually kind of induce a like a little cerebral vasoconstriction mechanism or it'll also inhibit the sphenopalatine ganglion how it does that we don't know but we just know in some way shape or form it causes a vasoconstriction of certain cerebral vessels and inhibits the sphenopalatine ganglion which was responsible for causing all that lacrimation salivation neurogenic inflammation all of that stuff like that right which would help to reduce the headaches a little bit so that's the kind of process there so big big thing here is give them oxygen in the form of a non-rebreather six to 12 liters per minute that is going to be very very important the next thing that you can add on is triptans so you can add on your triptans and we already kind of wrote these down uh your sumatriptan your zomatryptan okay generally these you want to give intranasal they've been kind of preferred or if they're given im iv or sub q okay generally uh these particularly though for triptans they're particularly im though they're primarily i am okay so we have tryptans again you can give intranasal or you can give intramuscular the next thing is if you this triptans aren't working so you've put them on a non-rebreather you've given them a triptan that didn't work you repeated the tryptan or you pick another type of drug and that's where ergots come in so it's the same thing as above for migraine so ergots and ergots is your dihydroergodomine and again this one can be given intranasal but it can also be given im iv and also subcutaneous so you put them on a non-rebreather you gave them oxygen you gave them triptans you either repeated the tryptan or you switched and gave them an ergot if that didn't work another option that you can consider is what's called intra nasal lidocaine putting like 10 milliliters of like a four to ten percent intra nasal lidocaine has also been shown to help with cluster headaches but either way the whole concept is that the tryptans and the ergots how do they work again they work by increasing 5-hydroxytryptamine i want this mechanism to be engraved in your your memories which induce that vasoconstriction mechanism and if you reduce the if you actually induce vasoconstriction that decreases the activation or that neurogenic inflammation which decreases some of the pain from the headaches or migraines and cluster headaches okay whereas intranasal lidocaine is just going to numb up the crap out of those trigeminal noise receptors all right prophylactic therapy if someone has again chronic cluster headaches where they're developing them very frequently and it's just it's extremely debilitating and you start treating them acutely and you decide hey i'm going to put them on some prophylactic therapy what am i going to give them well the drugs that have been shown to be relatively effective in this kind of scenario here there's two types the first one is varapamil so varapamil is a calcium channel blocker okay how this actually works in cluster headaches is not truly known maybe again it works by some special way here on the calcium channels of particular neurons that release vasoactive peptides cgrp substance p and inhibits that and inhibits the release of those types of neurotransmitters again this appears to be somewhat the first line medication and relatively effective in patients with cluster headaches another option to consider though is again your anti-convulsants these are not as effective as compared to verapamil but it's the same kind of thing do they work by inhibiting particular channels sodium channels that decrease the release of cgrp vasoactive peptide or substance p and again this includes to pyramid to pyramid or valproate okay so those are the two drugs that i want you guys to remember there all right so so far what do we have here prophylactic therapy our first line is verapamil okay calcium channel blocker second line would be kind of our anti-convulsants here like valproate or to pyramid the last thing that i want you guys to think about very important verapamil may take a little bit of time or the anticonvulsants may take a little bit of time to kick in so sometimes what may happen is you may bridge the patient and start them on prednisone to really reduce a lot of that neurogenic inflammation and this may act as a bridge until the varapamil or the anticonvulsant starts to kick in so you may put them on 50 to 80 milligrams and taper it over 10 to 12 days until the varapamil or the anticonvulsant kicks in all right that covers the treatment of cluster headache let's head at home ninja nerds and beast mode this on the treatment of tension headaches this one is actually the easiest one you can treat the episodic tension headaches which means that they occur generally less than 14 less than or equal to 14 times in a month or chronic which they occur more than greater than or equal to 15 times in a month either way episodic tension headaches you treat with nsaids okay you're trying to reduce the inflammation and so what were those drugs that we could give i could go through retimolic down but we already know them ibuprofen naproxen ketorelac a bunch of them right i could even offer acetaminophen so acetaminophen is another type of anti-inflammatory tylenol but you know what else is very interesting and has been shown to be very effective caffeine so caffeine has also been shown to be relatively effective in patients with tension headaches so nsaids acetaminophen caffeine sometimes there's even combos where you can give someone a combo of an nsaid and a caffeine combo or acetaminophen and a caffeine combo generally these are the measures that you would take in the acute treatment of tension headaches or the episodic treatment if they're having consistent chronic tension headaches how do you manage them the real only fda approved first line medication that has shown rct evidence to be beneficial is a particular type of tricyclic antidepressant which we already mentioned above and this is amma tryptolene this is the only one of these chronic therapy meds that has actually been fda approved and somewhat beneficial based upon rct evidence for chronic tension headache treatment the other ones that are more second line and don't have as much type of effectiveness based upon the rct evidence is other types of antidepressants and what are these these include mirtazapine and venlafaxine now the last thing that i want you guys to remember here is that when we're talking about tension headaches it's not always medical treatment sometimes it's just lifestyle modification remember i said with migraines sometimes with migraines you just have to put them in a quiet room a dark room let them calm down also with any of these avoid any triggers anything that could be triggering these headaches is also a good thing to do avoid eating lots of cheese and red wine and oral contraceptives if that possible chocolate and migraines right stop smoking stop drinking a lot of alcohol and cluster headaches and in trying to reduce stress and sleep more drink more water if you're dehydrated for someone who has a tension headache but again reversing the triggers are stopping those but the same thing with tension headaches is you also want to consider some type of cognitive behavioral therapy this has actually been shown to be very very effective in treating patients with chronic tension headaches other things that you can also consider is physical therapy maybe to relax some of those muscles or massage therapy and sometimes even chiropractic care has been shown to be somewhat effective all right so if you try to think about all of these things that are helpful for treatment of tension headaches again what was the big thing i want you to take away reverse all of the stop all the triggers get rid of all those things episodic insides acetaminophen caffeine for chronic the big one that i want you to remember is tricyclic antidepressants particularly amitriptyline i'm okay if you forget that one and then the most important thing is again chronic behavior cognitive behavioral therapy as well as other kind of measures like acupuncture chiropractic care physical therapy massage therapy things like that all right ninjas that covers headaches all right ninja nerds in this video we talk about headaches i hope it made sense i hope that you guys did enjoy and as always until next time [Music] you

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Published: Mon Aug 02 2021