DIP Episode 45 - Neurology Clerkship Shelf Review Part 2

Okay, welcome. My name is Divine. I am a PGOI1 resident, ultimately going into radiology. This is the 45th episode of the Divine Intervention Podcasts and this is actually the second installation of the neurogesial reviews. I'm gonna try to complete a series. Yeah, I do have a lot of content I want to go through, but yeah, I've been on a surgery reticion for the past like three-ish weeks and it's been a little more time-consuming than I imagined. So, as many of you that are listening to this probably, no surgery is not the easiest reticion in the world. Okay, so let's begin. So slide one, CSF findings in herpes meningitis and encephalitis, right? So the big thing I just want to draw here is that if you do a lumbar puncture in a patient that has like a herpes brain infection, classically, they would have a lot of red blood cells. So that's something you want to look out for. And usually the number of red blood cells are like less than a thousand. It's usually like 400, 500 on exams. If the number of red cells are like 4000 or 5000 or so must be a non-bacon number, you probably want to rethink the HSV thought and probably go more along the lines of a sub-recognite hemorrhage. And remember because herpes is a viral infection, right? Your white cells will obviously be elevated in the CSF, but you will not have a predominance of neutrophilus. You have a predominance of lymphocytes. And your protein will be mildly elevated, your glucose will be mildly decreased.

Okay, but most things will be normal. But remember, you have a lymphocytic pleusiteosis and you have a lot of red cells in the CSF. And I don't forget that herpes, right? It classically affects the temporal lobes of the brain, right? And usually if you take CSF, you can do like a PCR, like nucleic acid amplification of like CSF to meet the diagnosis of HSVME. You can also do viral culture, but most people just do PCR because it's just quicker, makes more sense to do. And obviously you treat HSV as a phyitis with E-cyclover. Usually give IV cyclover. And just one quick thing, I'll just chip in here, right? So just for if a patient has been in Gytis and they want you to think about some kind of like brain abscess as a complication, remember the classic trait of a brain abscess, right? So that's like fever, headache, and your allergic deficits. If you see those three things, and usually in the question, they will be very apt at pointing out that there is no nucleoregidity. Think about a brain abscess in that situation. Now the second question, the classic presentation of bacterium and in Gytis, right? So this is usually again a sodium onset, like nucleoregidity, really nasty headache, high fever, chills, you know, just the patient will certainly look toxic. And the CSF findings in bacterium and in Gytis, right? So it's a bacterial infection. So obviously your white count should be high and it should be a predominance of neutrophils, not lymphocytes, neutrophils.

TB is the only bacterium that is associated with an lymphocytic pleusytosis on CSF studies, at least that you need to know for the USML Es. I'm sure there's probably more. And so the white count is high in bacterium and in Gytis is predominantly neutrophils. The protein will be very high, right? And the glucose will be very low. Because again, think about that inflammation, those cells and bacteria and all that stuff, they're just chopping up the glucose. Now the most common cause of meningitis in neonates, right? That's group B strap. Remember group B strap causes most notable infections in neonates. And then if you're told about the classic cause of meningitis in a sexually active young person with skin ptki, or hopefully you're thinking about my serious meningitis, okay? Remember it's a gram negative organism. It's a gram negative diplococcus, okay? And the way you treat my serum and gyridism and gytis, right? You give safe tracks. And remember, safe tracks on is a third generation cephalosporing. Although in neonates, you don't want to give safe tracks on because it's associated with intra hepatic holostasis. So you want to give like baby safe tracks on under those circumstances, which is cephotoxin. And just while I'm on this right now, cephotoxin is a commonly is a common answer choice on exams for spontaneous bacterial peritonitis.

So it's just one of those all things you want to sort of keep at the back of your mind because it actually covers many gram negatives pretty well. Now, the way you treat, so I've talked about the way you treat my serum and gyridism and gytis, right? And one thing I'll just say is I actually talked about this in the anti-biotic guide, right? But if you have a neonate, right? Or like an infant that has meningitis, or you have a patient that's older than 50 that has meningitis, right? You classically give them a three-draw cocktail, right? So you give cephotoxin, right? You give vancomycin to cover stuff, or else, and like resistant strep pneumo. And then you give an picellin to cover elisteria, right? But classically, if a patient is like less than 50 years old and they're not like neonates, you can give them like cephotoxin and vancomycin and collider day. You don't necessarily need to give an picellin because listeria, as a cause of meningitis, is rare in that population. But remember, if a patient has bacterial meningitis, especially from strep pneumo, you also want to go ahead and add in steroids like dexamethosone. In fact, many times it's recommended that you give the steroids before the first dose of antibiotics. That actually helps with decreasing the morbidity and mortality, associated with bacterial meningitis, right? So like hearing loss after that episode.

And if a patient is a person is a close contact of a patient with an hycer meningitis, you actually want to profile out in those people, right? Remember, you can use one of three things and the way to remember that is RCC, okay? So the R stands for rifampin, the C stands for cephotoxin, and the second C stands for safe traction. Of all those if you've got an exam question with you, list that all three of those, go to rifampin. rifampin is the preferred agent. Now, my serobin and gyridis is actually preventable, right? I mean, generally, if you're about to go to school, so usually around like the age of 16, it's actually recommended by, I think it's like ACIP. It's like some comitiana immunization practices, or whatever it's called, right? They do recommend a niacere meningitis vaccination, because niacere is actually pretty rapidly fatal if it's not treated. You can see people like they have no corrigidity and boom, they're dead within 24 hours. Now, niacere, so what's your diagnosis? The patient becomes profoundly hypotensive, hypoglycemic, hyperchilemic and bleeds from every site, right? So hopefully you're thinking about a complication as a waterhouse, phrygics, and syndrome, right? So basically, this is just adrenal hemorrhage from involvement of, basically, like, bicere, like, finds its way to the adrenal glands. So you can basically have like a primary adrenal insufficiency from that, right? So if you're not making cortisol, right? You become hypoglycemic.

Remember cortisol is a diabetes hormone. If you're also not making cortisol, right, to become hypotensive, because remember cortisol has a permissive effect on the sympathetic nervous system. And then, because you're not making an outdoor serum, right, to become hyperchilemic, right? So if you go back to renophysiology at the level of the principal cell, right? Remember, sodium comes in through an inept channel. Potassium is extruded and wasted in the urine. That inept channel, its activity is promoted by outdoor serum. So if you have an outdoor serum deficiency, because you have a primary adrenal insufficiency from waterhouse phrygics, you don't reabsorb sodium, you don't create that negative charge in the urine site that draws out potassium. So you become hyperchilemic, right? And just as an aside, remember, if a patient has primary adrenal insufficiency, they'll also have a metabolic acidosis, right? Because that proton pump at the level of the alpha-intercaline itself doesn't work, right? So they will have a non-anion gap metabolic acidosis. And because it's a high-poil, those students, they'll be a type 4 reno tubular acidosis. And just as an aside, remember that if a patient is esplenic, right? If you don't have a spleen, you have a high risk of nasty, nasty infections with encapsulated organisms like an acere meningitis, right? So they describe like life-threatening meningitis in a kid that has like sickle cell disease, for example.

I think about strep pneumo for starters, but also don't forget an acere meningitis because it's actually an encapsulated bug. And also please do not forget that patients with terminal complement deficiencies, right? So like C5 to C9 deficiencies, they also have an increased risk of recurring nysereal infections. And one of the high-ealth thin, right? If a patient is being treated for PNH, right? Paroxysimon oxygenal hemoglobinaria with aculesumab, right? Remember, it's a C5 inhibitor. You are essentially inducing a pharmacologic terminal complement deficiency. It is actually recommended that those patients get my seramine injured in his vaccines, right? So they don't get life-threatening infections. Now, next slide says the next best step in management of a 25-year-old male who is actively having generalized tonic clonic seizures. He was started on intranasal dysmopressin, whoops, five days ago after a water deprivation test that was conducted at the local hospital, right? So dysmopressin is an ADHD channel lock, right? So this patient basically got a ton of ADHD, right? So they've reabsorbed the ton of water at the principal cells using the visopressin V2 receptors, right? So they essentially have hyponitremic seizures, right? So if a patient has seizures from hyponitremia, this is one of the few scenarios where hypertonic saline is indicated on tests. Usually they will make the sodium less than 120. The hotel is the patient is having seizures.

You do give hypertonic saline. No more saline is not going to cause it at this point. So you give hypertonic saline and remember that you don't raise the sodium by more than 12 million equivalents per liter within the first 24 hours, right? Because again, as you've seen, the later part of this slide, right? You don't want to reverse hyponitremia too quickly, right? If you've read first date for any reason, you probably remember the mnemonic that from low to high, the ponsal die and from high to low, the brain will blow, right? So if you crave hyponitremia too you can have osmotic dimylination syndrome. That's classicly known as central pointy malinoluses. You don't want that, right? Because that can present as the locked-in syndrome. Alternatively, for patients who have severe hyponitremia, right? You also don't want to correct that too quickly because that can cause like cerebral edema and then you can have like a trans-tentor herniation and the patient can die, right? So you also don't want that pretty much. So the general management strategy with electrolyte imbalances is you want to correct the electrolyte imbalance but you want to go slow. You never want to fix anything too quickly, right? You don't want to overwhelm the body's homeostatic responses. Now the next slide, bizarre dreams just after getting up from sleep, right?

So that's a hypnopompate carrosination and just before going to sleep, that's a hypnogodject hallucination and then it's the tell you that the patient has a history of three major accidents from falling asleep at the wheel. Oops. Plus sudden falls from low extremity weakness, right? So that's kind of plexi, right? So if you see all these things together, I really hope you're thinking about narcolepsy, right? And the way you make the diagnosis of narcolepsy, right? Just like any other sleep disorder, you have to do a sleep study, right? So the buzzword you're looking for in exams is polysomnography and your findings on polysomnography, right, is that they will have a decreased sleep latency. So those are the kind of people that lie on the bed and boom, they go straight into REM sleep. And the way you treat narcolepsy, right? You can do a couple of things, right? So they should have like frequent nubs during the day. You can give them stimulants like more daffinia, right? That can help with like making them like wake for during the day if you're making. If for the cataplexia, right, where they have like sudden loss of muscle tone, usually on exams, the answer they go after is sodium oxybit, but you can actually use tricyclic antidepressants and SSR Is for that purposes, right? But on exams, think mostly about sodium oxybit. And in terms of CSF deficiencies, in patients with narcolepsy, they actually have low levels of something known as hypochritin, okay?

Hypochritin levels are low in patients with narcolepsy. Now, while we're on that thought, right, what's the drug that's used in the treatment of insomnia that utilizes this pathophysiology, right? So the drug is known as a severe accent, right? So think about it this way. If having a hypochritin deficiency makes you sleepy, right? AKA have narcolepsy. You can imagine that if a patient is an insomnia, maybe blocking hypochritin receptors, right? To sort of like pharmacologically induce a hypochritin deficiency could make those people sleep better. That's how severe exa-works. I believe it's known as Belsomera. If I'm not mistaken, that's like the trade name. It's basically a hypochritin receptor blocker that's used to treat insomnia. And again, I've talked about how you treat cataplexia in narcolepsy. Okay, so next slide. A severe headache plus multiple extracurricular muscle deficits plus a recent his travel tightest media. This is something you probably just want to be able to recognize on a test, right? So this is carbonous sinus thrombosis. Okay, remember the carbonous sinus transmits a lot of the cranio nerves that are associated with innerviting the extracurricular muscles, right? So like in the middle of the carbonous sinus, you have the internal corollid artery traversing with the abducense nerve. That's cranial six. Remember that controls the lateral rectus muscle, which is involved in a B-duction of the eye abduction.

Okay, and then on the side of the carbonous sinus, you have cranial nerve three, right? And then you have cranial nerve for the trochlear nerve that does the superior bleak muscle. And then you have cranial nerve V1, right? So the ophthalmic nerve, and then you have cranial nerve V2, that's the maxillary nerve. Okay, those are all transmitted through the carbonous sinus, right? And again, the all-control many multiple extracurricular muscles. So if you describe a person that recently has had like an operator's return infection, or like a head and neck infection, and then they tell you that they have all these extracurricular muscle deficits, you really want to think about a thrombosis of the carbonous sinus. And one reason that you can get thrombosis of the carbonous sinus is that has like this very like intense and asthmosis, with like ophthalmic veins that sort of supply some of the paranysal sinuses. So infections can very easily make their way from like your respiratory apparatus to the to the carbonous sinus. And the most common organism actually that's implicated as a cause of carbonous sinus thrombosis is staph-orius. If I'm not mistaken, the second most common cause is strep-numon. And really the way you treat carbonous sinus thrombosis, you give antibiotics, okay? And then you also give heparin because it's a thrombotic disorder, right? And if you then we're together and so this is probably more something like a shop on a neural shop or a medicine shop even. Right?

So like severe headache, necrotic sinusitis, an apision with a blood glucose of 300, a pH of 7.13 and a bicarbon of 15, right? So this is a patient in decay. So hopefully you're thinking about mucomicosis, right? So like rhizoposal, mucus species, basically the way you treat this is you have to like go in and do a bridge and then give those patients some footerabone, okay? I'm footericin B. It's like the only drug that can basically rescue these patients because this has a very high morbidity and mortality. Now next slide, the classic presentation of Parkinson's disease, right? So Parkinson's is associated with like an asymmetric resting tremor, right? There's also like the cogwheel rigidity, there's the fascinating gate, right? And then there's the postural instability. Those are like the classic findings in Parkinson's disease. But there's other things you also find in Parkinson's disease, right? So like small handwriting, right? So the buzzword is micrographia. They have like orthostatic hypotension, right? Because they have like autonomic instability and stuff like that, okay? And really the pathophysiology of Parkinson's is you essentially have a destruction of the dopamine producing cells in the substantione migra parts compact, which is a part of the midbra. Okay? And another potential thought behind the pathophysiologies, people believe that low body, right?

So those things that are made of alpha-synuclein, they sort of build up as intracellular inclusions in the dopamine producing cells in the substantione migra. And remember, if a person has like abnormal inclusions in a cell, that can actually ultimately lead to ultimately lead to cell death. So just something to keep in mind. And again, it's you have a deep pigmentation of the substantione migra. That's the gross finding in Parkinson's disease. And Parkinson's has a lot of treatments, right? So usually if a patient has like early Parkinson's, you want to go ahead and not jump straight to carbidopa-livo-dopa. You usually start with like a manadine, right? A manadine is a drug that was used to treat the flu before. But apparently it increases the release of dopamine in the central nervous system, right? So you can start with a manadine. You can start with a dopamine agonist, right? So like you can start with a drug like bromocryptine or carburegoline. There's drugs like primatexol, epomorphine. Those are all dopamine agonists. They can actually be used in the initial treatment of Parkinson's. Alternatively, you can use an ammonium inoxidine as being better, like a cellulogen or a satcheline. Remember, mon aminoxid is B, selectively breaks down dopamine, okay? So by inhibiting that enzyme, your dopamine levels are sort of boosted. You can treat Parkinson's. One other thing you can do is you can also use drugs like entakapone and tokapone, right?

So remember, those are your comtein inhibitors. Entakapone works mostly in the pair. It works also works in the brain, but its major job is in the periphery. It doesn't cross the blood brain barrier as much as tokapone. Tokapone has like a longer half-life. It's an awesome drug, works great in the brain, works great in the periphery. Only problem is that tokapone also can explode your liver. So many people prefer to use entakapone for that purpose. I mean, for that reason. But yeah, early Parkinson's, you basically try to use everything other than kabi dopa livodopa. Kabi dopa livodopa is what you can use as a last line because it works for a few years. And then it essentially becomes ineffective, right? Because of the on-off phenomenon that I discussed in the neuro-phomacology podcasts. So that's how you treat Parkinson's and not share. And the classic causes of drug-induced Parkinsonism, right? So you want to think of like your neuro-laptics. Remember, those are dopamine receptor antagonists. You want to think about drugs like metoclopromide and don't peridone. Remember, those are used as anti-medics. And they also used to treat gastro parisis, classically in diabetics, right? So they have dopamine receptor blocking activity. So they could be used for those purposes. I mean, they could cause a drug-induced Parkinsonism. And then the anti-colonergic that reduces tremors in Parkinson's, right?

So I remember from the neuro-phomacology podcast, I essentially established an equation if you make that helps with the understanding dopamine from ecology. And this equation was that dopamine and acetylcholine have an inverse relationship. So the patient has Parkinson's, right? They have low dopamine. So if dopamine is low, acetylcholine is high. And from those neuro-phomacology podcasts, I sort of described how having high levels of acetylcholine may be associated with dystonias. So if a patient has like tremors in Parkinson's disease, right? You want to go ahead and give drug-like benz-stroping. Ben-stroping is a most chryseptic and antagonist that could help with the tremors in Parkinson's. If they describe a question, this will probably be more of a side-shelf question, but Parkinsonism and a young patient that took a drug at a party, right? You want to think about like improperly cooked opioids, right? So that potentially contain MPTP. MPTP is toxic to the dopamine, allergic dopamine producing cells in the substantial Niagara. And in Parkinson's disease, right? On histology, you see like alpha-synuclein, right? So like, Louis bodies, they're like your synophelic inclusions of alpha-synuclein. And I've talked about the super high-youtside effects of levodopath-cabidopath, right? Those are the on-off phenomenon, right? So like, it takes a while to work and then when it works, it just works for a short period of time.

And I've talked about how you treat early Parkinson's disease. And remember, Parkinson's is a resting tremor, okay? An essential, and it's an asymmetric resting tremor, and it gets better with activity, the tremor in Parkinson's. Contrarily with an essential tremors, an essential tremor is symmetric versus Parkinson's that is asymmetric. Essential tremors actually get worse with activity, and actually the essential tremors respond really well to propoundal. Now, if a patient is taking in the dopamine antagonist, right? So like a neuroleptic, right? And they have the stonias, right? You generally want to give a powerful anti-colonergic-like bench-thropping, or you can give an anti-histamine like diphenhydramine that has significant anti-colonergic activity. Another thing I also want to mention is, I'll just mention it here because it just comes up quite often on exams. If a patient has like a focal dystonia, so not like a generalized dystonia, like a focal dystonia, so let's say like one part of their face has like a dystonia. Actually, the treatment of choice under those circumstances is like Botox, right? Because it can sort of quiet down those muscles because you cause a decreased release of acetylcholine at the neuromuscular junction, so those muscles don't fire, right? So again, you sort of remember when I said that acute dystonia is as high levels of acetylcholine, so that sort of ties in there.

Because by giving Botox, the botulinum toxin decreases acetylcholine release at the neuromuscular junction. And classically, like those focal dystonias, they describe it as been associated with, I don't really know how to pronounce the word, but it's called like a gest, like G-E-S-T-E, where they say like, oh, if they sort of massage the area, the dystonia sort of goes away, just sort of keep that in mind, but classically, you treat a focal dystonia with Botox. And then a relatively tricky question that comes up quite often on NBM easy, if a patient has a Parkinsonism and their psychotic, right? So if a patient has like Parkinson's, right? Those people already have low levels of dopamine, but if they have psychosis, you're like, hmm, how do I treat the psychosis? Because classically, psychosis is treated with dopamine receptor blockers, right? But you obviously know that's not a great thing. In a patient that has a disease like Parkinson's that's associated with dopamine deficiency, if you may. So for those patients, what do you classically do on exams is if they told you in the acute stem that, oh, they recently bumped the adose of carbidopa levodopa, you may want to scale back the dose, but if that's not an answer to, if that's not an answer to, you may want to consider giving a, um, quityapine, it's an atypical anti-psychotic, but it has very weak dopamine receptor blocking activity.

It's usually not a bad choice for the treatment of psychosis in a patient with Parkinson's disease. And then finally, if a patient with Parkinson's disease has a hypertensive crisis, right? You're thinking of that patient potentially being on an M-A-O-B inhibitor, like a cellulogen or a sagelline. Yes, I said those drugs only break down dopamine, but they also break down other kind of colomites, okay? So you want to be careful. You don't want to combine like, uh, they can classically give you a question about a patient that has like Parkinson's and they have depression and you're trying to give them like an M-A-O-I, like phenylzene or trineylcepromine or isocarboxazet. That can very easily trigger a hypertensive crisis. And remember, those hypertensive crises, you treat those with a phentolamine, basically you give an alpha-1 blocker. Now, next question, 35-year-old female with a BMI of 35 plus visual difficulty, plus in term-ethane severe headaches plus treatment for acne-wall garris, right? So hopefully, you're thinking about pseudo-tomorceribrate. The new term is idiopathic intracranial hypertension. I hear when they change the names of things, but I-I-H or pseudo-tomorceribrate, right? And basically, I just give you like the classic risk factors, right? So like obese female, it, pseudo-tomorceribrate can show up in guys on tests, but can show up in guys in the real world, but not on MBM Es. It's almost always in a female, okay? With a large BMI, okay?

And they have visual difficulty because of those increased pressures, especially around the optic nerve. And usually in exam questions, they'll tell you that they have like signs of a papillodymorna on a fondoscopic exam. And vitamin E derivatives, right? Classically, they're used to treat acne-wall garris, also like risk factors for eye-eye heat, right? Also tetracycline, based on type biotics, also have that as a risk factor. I mean, also risk factors for the development of pseudo-tomorceribrate. And the way you make the diagnosis is usually, like you see like signs of papillodymorna on a fondoscopic exam, you're like, oh no, this patient has increased ICP, so you do a CT scan first, right? But you do the CT scan, things look relatively normal, right? So you then do the LP, and you see the elevated opening pressures. Usually the cutoff is like 250 or something like that. If you see elevated opening pressures, that's pseudo-tomorceribrate. And generally, you can treat it with like a lumbar punctures, like therapeutic lumbar punctures, alternatively you can also give acid a zolomide, right? To decrease the production of CSF. So next slide, because I'm sort of scared that I may be pitched for something soon. So let me quickly run through this. Okay, so for the one-year old male presents with a one-year history of forgetfulness and behavioral changes, his father had a similar presentation before he died at the age of 47, right? So this is haunted, okay?

Remember, it's a trinucleothide repeat disorder. And the pathophysiology, right, involves you basically have degeneration of the strideum. If you want to be a little more specific, it's the codic nucleus that atrophys in Huntington's disease. And remember, it's as we see, they would see agey repeats, okay? It's a chromosome 4 issue. And it's a dosomodominant inheritance, and it actually illustrates the genetic principle of of anticipation. Where like you get a more severe presentation and an earlier presentation, as you go further in, as you create like new generations. And really the way you treat Huntington's is with things that have anti-dopamine activities like hollow peridol, okay? You can give tetrabenazine. Remember, tetrabenazine is a v-matin inhibitor, so that basically depletes your pool of dopamine. And one other thing I just want to say, because I think someone asked me this question recently, it's usually pretty annoying to memorize like, oh, this disease is a dosomodominant. This disease is a dosomodorescensive blah, blah, blah, blah, blah, blah, blah, blah, so it's pretty annoying, right? But the thing is there are some general principles that may help. They don't work all their time, but they work pretty well. Most trying nucleothide repeat disorders are a dosomodominant inheritance. They're like two high yield exceptions, right? If I remember incorrectly, phrygxy-taxia is one. That's a dosomodorescensive inheritance.

And then fragile syndrome, fragile x has an x in the name, right? So that should hopefully help you remember that it's like inherited in an excellent fashion. Many structural disorders, right? Also inherited in an dosomodominant fashion, right? So like morphans, that's like a structural protein disorder, hairdressers, cytosis, that's a structural red blood cell disorder. That's classically inherited, those are classically inherited in an dosomodominant fashion. And then enzyme defects, right? That's classically inherited in an otosomodorescensive fashion. Okay? So hopefully those principles kind of help you remember just sort of like make educated guesses on exams. Now, slide nine, worst headache of a patient's life. This is a sub-racrondemory, right? And in the question I say, on physical exam, bilateral flank masses are palpable, right? So this is basically ADP-KD, or a dosomodominant polycystic kidney disease. Remember, these patients, classic Lyon exams can have aneurysms in the circle of willis, right? Most commonly in the anterior communicative artery. And the murmur that you'll school theta, the apex between S1 and S2 is mitrovov prolapse, okay? Remember, mitrovov prolapse has an association with ADP-KD. And really, the next best step in management, right? Because this is a sub-racrondemory, this is a hemorrhagic stroke. The first thing you do is this non-conhead CT, right? So the CT is kind of the head without contrast.

And usually they'll show you blood like a hyperdense lesion, right? You see that and you're like, oh, okay, brim bleed, hemorrhagic shock, right? I mean, hemorrhagic stroke. So you generally like try to decrease blood pressure and all that stuff. But assuming like you have a strong suspicion for sub-racrondemory gender head CT, the non-conhead CT is negative, you want to go ahead and get an LP, right? I think you're looking for a zanctochromia, right? Since the LP is actually pretty sensitive for a sub-racrondemory. So if you have a negative non-conhead CT, you'll proceed to a lumber puncture and you're looking for zanctochromia. And the treatment strategies, again, you try to lower blood pressure, you try to keep it like around like 140 over like 90 or something like that. You don't want it higher, right? Because you don't want like more hemorrhagine in the brain. Please don't give TPA for a hemorrhagic stroke. You have a loss on your hands. That's like not prudent. And then, because I mean, right, you don't want to give a clot, the loss of a person is bleeding, right? That doesn't sound like a very good idea. And then preventing supraimposed ischemia, right? You want to give a dihydroperidine calcium channel blocker. Classically on exams, that would be Nymodepim, okay? Helps pretty well with preventing post-struct visospasm. Post hemorrhagic stroke visospasm that can sort of trigger like supraimposed ischemic stroke on the hemorrhagic stroke that just happened.

Now, the final slide, the headache syndrome, right? So cluster headache, right? So this is the headache that is usually associated with like rinoria, right? Like unilateral, like rinoria, and unilateral, like congenital, like injection, right? So like tearing and all that stuff shows up at like the same time every day for days or weeks on it, right? Tension headache. And remember a cluster headache, right? You can avoid it very quickly with inhaled oxygen. Tension headaches, these are the ones you get from studying too hard, basically, right? So it's usually like bilateral, it's worse at the end of a hard-dease job, let's say like gonna surgery rotation, for example, or you're studying for step two, seeker step one, and then those usually respond to end sets, right? And then a migraine headache, right? It's the one that's usually treated in lateral, but it could be bilateral. It may or may not be as either than r, most migraines are not associated with r's. My migraine right is classically worsened by loud noises and louds like bright lights, right? So like photo and photophobia and photophobia, and it's usually pulsata, right? And basically, vision has to like rest in a dark room to sort of feel better, right? And remember migraines, right? If a vision has an acute migraine attack, you can treat that with somatriptin or gotamine, right? So somatriptin or gotamine, remember somatriptin is a serotonin receptor, um, oh this is weird, this is not good.

Soatriptin, if I'm not mistaken, it is a serotonin receptor antagonist. Wow, this is terrible. I love pharmacology. How do I not know the mechanism of action of somatriptin? But yeah, for now, say it's a serotonin receptor antagonist. Yeah, I remember. It's a serotonin receptor antagonist, um, yeah, because it can trigger serotonin syndrome, that's how I remember. So it's a serotonin receptor antagonist, okay? It's used to acutely treat migraines. So here's what you'll try to do to your own test. It tell you, oh, a patient has more than 8 or 9 migraine attacks a month, right? So more than 8 is like the cutoff for where you need to profileax these people. And then they try to trick you into giving somatriptin for profileaxes, that is not a good idea, right? So, um, if a patient has an acute migraine attack, you can give a regutamine, you can give somatriptin no issue. But if you're trying to profileax against migraines, uh, classically on the example, you want to give perprenolone, okay? Nonselective beta blocker. Uh, remember, you don't want to give that to a patient or the histiobasmer, right? That's not a, uh, stellar idea because you can get a bronchoconstriction and that'll be back. Um, alternatively, you can also give like, um, uh, topiramate that also works on tests. You can give a tricyclic and titanipresent, right?

Although remember, um, so like more triptoline, image triptoline, remember, you want to avoid that in like the elderly or you also want to avoid that in patients with a histioblochoma because tricyclics have anticholinergic activity so they can cause my dry asses and decrease drainage through the canals of schlep. Um, so profileaxes migraine, like chronic profileaxes migraines, beta blockers, tricyclics, you can give uh calcium channel blockers, you can give um, um, uh, topiramate. Remember, topiramate is associated with a nephrolethyasis and like mental slow side effects. Uh, but acute treatment or got a mean, so much rep fan, that's all good. And then an agisic rebound headaches, just a person takes a ton of an agisic, you have headaches, you need to just win them of those an agisics. It would not be pretty for the first few days but it will get better as time goes up. Um, and then headache and mental status changes in December in an 83-year-old female who uses an old space heater, right? So hopefully you see this as carbon monoxide poisoning. Um, I mean generally, right, you want to go ahead and uh, give like hyperbaric oxygen or like high flu oxygen, right? Because that decreases the half life of um, carbon monoxide bound to um, to hemoglobin, right? And remember for these patients, a poor fox is not a great idea on the test. Um, because I mean, poor fox does not distinguish between oxygen bound to hemoglobin.

So basically, those not distinguish between hemoglobin that is saturated with an oxygen versus hemoglobin saturated with a carbon monoxide, okay? So you generally want to check carbon monoxide hemoglobin levels and that will give you a more definitive diagnosis. And this is just the low yield, it's like low yield, but it's just one of those bizarre things that we pop up on an exam. Remember that carbon monoxide poisoning is actually associated with hyperintens lesions in the global spallidus on imaging, on MR imaging, just one of those bizarre things, you just want to file a wind your mind for the future. Now, right side of headache in a 35-year-old smoker that has occurred every day around 90 M for the past month and blah, blah, blah, blah, I already talked about this. That's a that's a cluster headache, right? And then the high yield contraindication to a common migraine met, right? So basically here I'm talking about so much trip time, right? So the contraindications, right? So remember, I believe I mentioned this in the neurophomacology podcast that viso-construction is good for headaches, but its viso-dilation is bad for headaches, right? So, so much triptom, right? Image tracks, basically. It's a serotonin receptor agonist, it can cause viso-construction. So much triptom is not good for people with a histro-viso-spastic disease, right?

So if a patient has a histro-like prins metal, angina also called, at least the new term is variant angina, you don't want to give them so much triptom. If they have coronary artery disease, no so much triptom. If they have like crest syndrome, right? Like renautphenominone, no so much triptom. That's not a good idea because they all have a viso-spastic disease. So much triptom is a viso-constructor, not good for those people. And then because so much triptom is also a serotonin receptor agonist, remember it could trigger serotonin syndrome, right? So you don't want to give like so much triptom with like linesolid, for example, which is an MEUI, right? Because if linesolid being a weak MEUI, it can sort of boost your levels of serotonin, right? You also don't want to give so much triptom with like an SSRI or an SNRI or an MEUI or tricyclic or what else? There's one more drug I'm thinking about. Come on, thank, let's see. Sorry, I'm sort of giving this for memory. Yeah, the MEUI being inhibitors, that I used to treat Parkinson's, right? Again, yes, those inhibitor prevent the breakdown of dopamine imprimary, but you can also get into trouble with those because they also, at least partially, bring down some kind of colomites. And then actually another unusual one is like, entacapone, tocapone, right? Yes, they are contain inhibitors, but they can actually also trigger serotonin syndrome.

So again, the short just here is you don't want to mix two serotonergic medications together. So this is the end of today's podcast. I will pick up with, I'll probably pick up with this in the next podcast. I'm just going to try to make a series of podcasts to sort of finish up this a neural shell review. So this is part two. Look out for part three in the future. I'll have to go now. Thank you for listening. If you have any questions, please drop me a line. Hopefully after my surgery or t-shirt, I should be able to pump out more more content because I certainly have a lot of content in my mind is just literally no time to do this. I mean, many of you know how surgery rotations go. So have a wonderful day. It's an early day on Monday, do your best, work hard, and God bless. Have a great day. Bye.

Asymmetric resting tremor, cogwheel rigidity, and postural instability.

Lymphocytic pleusytosis and a high number of red blood cells (RB Cs).

Infection with Neisseria meningitidis (Meningococcus), leading to bilateral adrenal hemorrhage.

Non-anion gap metabolic acidosis, specifically a Type IV Renal Tubular Acidosis (RTA).

Rifampin (as part of the R-C-A regimen).

Decreased sleep latency, indicating rapid onset of REM sleep.

Obese female and high BMI.

Encapsulated organisms like Neisseria meningitidis and Streptococcus pneumoniae.

Essential tremors are symmetric and worsen with activity; Parkinsonian tremors are asymmetric and rest.

Dexamethasone (steroids) and prompt administration of appropriate antibiotics.

It decreases the production rate of cerebrospinal fluid (CSF).

Huntington's disease (CAG trinucleotide repeat expansion on Chromosome 4).

Cluster headache.

Xanthochromia.

Encapsulated organisms like Neisseria meningitidis and Streptococcus pneumoniae.

Essential tremors are symmetric and worsen with activity; Parkinsonian tremors are asymmetric and rest.

Dexamethasone (steroids) and prompt administration of appropriate antibiotics.

It decreases the production rate of cerebrospinal fluid (CSF).

Huntington's disease (CAG trinucleotide repeat expansion on Chromosome 4).

Cluster headache.

Xanthochromia.