DIP Episode 47 - Neurology Clerkship Shelf Review Part 4

Okay, welcome. My name is Divine. I am a PGI1 resident. Welcome to the 47th episode of the Divine Intervention Podcast. I'm going to continue with our review of neurology for the clerkship. So let's begin. Slide number one, a student in a lab is on newly touching a life-thed Bunsen burner in the chemistry lab until his hand is pulled away by the TA. Physical exam is notable for loss of pain and temperatures in session in the upper extremities bilaterally and mild hand muscle weakness. What's your diagnosis, right? So this is obviously a syringomile, right? So this is pain and temperature loss in a in a keep-like distribution. And the path of physiology basically involves an obstruction in the spinal cord of the central canal. So when you obstruct that central canal, you then have like a cystic expansion of the central canal above it. And with that cystic expansion, you can basically begin to compress on the anterior white commission. If you compress on the anterior white commission, you basically knock out the spinal thalamic tracts bilaterally. Right? So because remember the spinal thalamic tract after it, you have the first synapse like through the tract of Lissauer and they use synapse in the posterior the posterior horn of the spinal cord. You then ultimately bring fibers that cross in their anterior white commission before it ascends contralaterally in the lateral brain stem.

So if you have expansion of the central canal, you'll damage the anterior white commission, you knock out your spinal thalamic tract. So bye-bye, pain, temperature, and uh, pain-prick sensation bilaterally. And then the mild hand muscle weakness. Basically, the thing that happens is as time goes on, if the compression like worsens, worsens, worsens, and you extend beyond the anterior white commission, then you begin to damage the ventral horn of the spinal cord. Right? And the thing is the muscles that control your upper extremities, at least the low motor neurons that control your upper extremities, they are found very relatively close to the anterior white commission. So you begin to have like hand muscle weakness. And because this is a spinal cord pathology, you do actually make the diagnosis with MR imaging. So you use an MRI and you can make the diagnosis that way. So next slide, no core rigidity in a recent immigrant presenting with hemoptysis and high fevers. There is marked enhancement of the base of the brain. That's the high-octerminology here at the base of the brain. So they should tell you that this is TB, right? And obviously for this, you want to do a lumbar puncture. And in the lumbar puncture, remember TB is in fact a bacterial infection, but one of the big things you want to keep track of here is that the CSF studies will show predominance of lymphocytes, right? So your bacterial infection, but you'll see you have an elevated white count.

And the thing that will be elevated will be lymphocytes. And the CSF pressures will be opening pressures will be high, okay? The protein content will be high as well because there's a lot of inflammation. The glucose level will be low, okay? So really like TB meningitis is just like any other kind of bacterial meningitis. The only big difference is that instead of having a predominance of neutrophil, so you have a predominance of lymphocytes. And in terms of your... So those are basically your findings on diagnostic testing, right? And I mean you probably want to do like some kind of like culture of the CSF, right? Or you can do like the acid fasting, right? So the zionylsynstine to identify TB. And in terms of treatment, right? You want to go ahead and give like the ripe regimen, right? So like rifampine, remember that's an iron polymer, is inhibitor. You want to give isoniasid, remember that can costate a rubblastic anemia. You want to give pure zenamine. Remember that works pretty well in acidic tissue. And you want to give an ethambutol. Remember ethambutol can cause problems with like coloblininess. So you want to keep track of those. And then you also want to give vitamin B6, right? Pyrodoxyl phosphate to prevent the peripheral neuropathy. That's associated with isoniasid because remember the enzyme that converts glutamate to GABA, GABA decarboxyl leaves uses vitamin B6 as a cofactor. And isoniasid depletes vitamin B6.

So you have less of a cofactor in the conversion of glutamate to GABA. So if you have less GABA more glutamate you could potentially have seizures. And then in some cases some, you'll see some text that actually say to give steroids as well in the setting of TB meningitis, it keeps changing all the time. But for sure for sure, by determining Gitis you do need to give a dose of dexamethosone. Usually before you even give your first dose of antibiotics. Now the way you differentiate meningitis from encephalitis is usually on exams. Encephalitis, those people tend to have more in the way of neurologic deficits. They don't usually have, they may not necessarily have no corrigidity. So just to keep that in mind. What I mean encephalitis is inflammation of the brain itself. Meningitis is inflammation of the meninges, not necessarily the brain, a parenthema. Now next slide, the most common neurologic sequela of meningitis in kits, that's actually hearing loss. And the top three causes of meningitis in neonates, right? So there's a simple numonic for this, it's known as gel, G-E-L. So the G's for group B strap, remember group B straps causes essentially an innotable infection in kits, at least in neonates. So the first 20 days of life, the E stands for equal light and then the L stands for listaria. In terms of treatment strategies, in general for a neonate, they ask you what you would want to give empirically for suspected meningitis on tests.

You want to go ahead and give sephaltoxin, right? So they will try to give you an answer that tends you to choose sephatraxone. Do not choose sephatraxone because sephatraxone can actually cause, like intrahepotacolistesis in kits, so you don't want to do that. So basically give like the third gen baby sephalospory. In that case, that'll be sephaltoxin. So you give sephaltoxin, you give then komisin and you give them pysilin. The ampysilin helps you cover the ampysilin helps you cover against listaria because that's like the drug that has been shown pretty consistently to cover listaria. An alternative regimen could be then komisin and gentomisin, so sort of keep that in mind. But that's less common on tests. And then CSF studies in bacterial meningitis, right? So again, elevated white count, it'll be a predominance of neutrophils, protein will be high, right? Glucose will be low. If it's viral meningitis, things are relatively normal, right? So your opening pressure is not too high. You have a, you have a, you have a mildly elevated white count, but it'll be primarily lymphocytes, right? You have low-ish glucose, right? So like low-normal glucose, you have like high-normal protein. Basically, things are like mostly normal, environment, and genties, where you see a ton of lymphocytes. And then for phongo meningitis, right? That's essentially like botermin and gentis, right? So the thing is, if you notice, I'm trying to group things here for you. That's the thing.

You don't want to just memorize things blindly. Try to group things. It's much easier to remember. Just basically remember the findings in botermin and genties, and then remember that it's non-neutrophils that I elevated. It's lymphocytes, and that's all you need to remember. Now, CSF studies in a patient with symmetric asendin paralysis after a recent viral infection, right? So a bloodied viral infection, right? So hopefully with the symmetric asendin paralysis, you're thinking about Guillembris syndrome, right? So this person potentially had a Campylobacter infection, and Campylobacter does cause bloodied area. It's associated with Guillembris syndrome, right? So that Guillembris syndrome where you have like symmetric asendin paralysis. And the big thing I just wanted to point out here is the CSF finding of abumino cytologic dissociation, abumino cytologic dissociation. It's a classic finding in Guillembris syndrome. And one of the things you also want to keep track of on this slide, right? So the question here says CSF studies in in a 30-year-old female with an afferent popularity effect and other neurologic deficits, right? So this patient has multiple sclerosis and a multiple sclerosis, right? The thing is you'll find something known as oligoclonal band, oligoclonal bands on CSF studies.

So that's one thing you want to keep in mind, oligoclonal bands, although really the way that MSS diagnosis with MR, it's with an MR, it's a radiologic diagnosis, it's diagnosed with an MRI. And just to I guess add some a little more context with the albumino cytologic dissociation is, the thing is if you notice, when we talked about the CSF studies in meningitis, right? For like bacteria, for example, I said, oh, the protein will be high and the white cell count will be high. The thing is usually when the white cell count goes up, the protein content goes up. That's usually the trend, okay? But if you look at a person's CSF study and you're like, wait, the protein amount is really high, but the white cell count is almost nonexistent. There's no agreement between the white cell count and the total protein content, right? That concept is known as albuminocytologic dissociation. There is no agreement between the number of white cells you're seeing and the very elevated number of proteins you're seeing in the CSF. That is a pathomomonic finding on exams with Guillembrille syndrome. And then if you see CSF with a ton of red cells, where you're thinking about her piece, right? HSVN, HSVN Sephalitis. Remember that classically affects the temporal lobes. Although if you see like 5,000 red cells in a patient CSF and the present with like no coregidity and severe headache, you probably want to think more about a sub-acnotic emerge as against meningitis.

Now next slide, general treatment cocktail for bacterial meningitis, right? So just remember CVS, like CVS, like the pharmacy, right? So the C4ceph triaxyl, okay? You want to cover an aceremin and get rid of this with that, the V4 vancomycin, and then the S4 steroids, okay? You want to give the X Methosol to reduce the morbidity and mortality associated with inflammation. And if you're dealing with the elderly, you generally want to add ampeicillin, right? So like the elderly, people that are immunocompromised, people that are super young, you want to go ahead and add ampeicillin because that will cover the stear, because the stear is almost 100% fatal if it's not treated. And again, I've sort of repeated this on the previous slide, right? So like CSF studies with normal glucose, slightly elevated protein, and lymphocytic pleusytosis, that's a viral meningitis, right? And then HSVN, meningitis, or encephalitis, right? We'll show like enhancement in the temporal lobes of the brain, that's like the big ones where you want to remember. Now, next slide says a 25-year-old male presents with a temperature of 103 severe headache and a 2-day history of profound low extremity muscle weakness. It was recently treated for otitis media. So this is a high-ealt triax to be aware of. In this QSTEM, the triad you want to sort of like lock down in your mind is fever, headache, and neurologic deficits. I'll repeat it again, fever, headache, and neurologic deficits, okay?

Fever headache, neurologic deficits, that is a brain abscess. That is the classic triad of a brain abscess. And usually in the QSTEM on NBM is, they'll be very careful to tell you that the patient does not have no colg rigidity, okay? So that's the triad for a brain abscess. Now, the way you make the diagnosis, right? Is you doing MRI? An MRI shows a brain abscess really well. And you basically treat it the same way you treat meningitis. But it's just some key considerations to keep in mind is you usually try to incise and treat, like you usually try to treat the abscess, that's one. And then the second thing you try to do is you also give steroids, especially if the abscess is causing like compressive symptoms, you want to give steroids to decrease the, decrease the swell so that the patient does not have to remove and die. And then the bug again, meningitis, MRI, and has met at the base of the brain, that's TB. You feel the right regimen and vitamin B6. Now, next slide, a 35-year-old zoologist is brought to the ED by ambulance after becoming unresponsive at home. He studies cave duallyn animals. So, I don't know, maybe bats, who knows? Over the past two weeks, he has resisted, attempts by his parents to give him water or get him to the shower. That's bad news right there. This is rabies, right? This is rabies.

And really, the way you would have prevented this is assuming he knew when he was bit by like a bat or whatever organism that was carrying the rabies virus, would have given him like the rabies immune globulin and would have given him the rabies vaccine. And actually, one bizarre thing that may show up on an example of the blue, that I feel like will stump a lot of people, is the fact that you give the rabies vaccine and the rabies immune globulin at two different spots. You do not give them at the same spot to a human being because the immune globulin will just bind up the vaccine and then the immune globulin, yeah, and then the vaccine will basically not mount an immune response. So you don't want to do that. So you give them at two different sites. And the pathonomonic histologic findings, right? Those are negribodies. Negribodies, they're like pink, your synophilic bodies, that you'll find in neurons, pathonomonic for rabies. Now, next slide, bilateral acoustic neuromas, right? So the syndromic association, hopefully you're thinking about NF2, right? I talked about NF1 in the previous podcast. So NF2, neurofibromatosis type 2, okay? And again, it's a neurocutaneous disorder. This principle doesn't always work, but it works pretty well for the most part on NBM Es is, most neurocutaneous disorders are inherited in an autosomal dominant fashion, okay? And the gene product is merlin, okay? And the mutation is in chromosome 22, okay?

So just to keep that in mind, so chromosome 22, merlin, autosomal dominant inheritance, NF2, classically associated with bilateral acoustic neuromas. Some people also call them vestibular schwanomas. And then the involved cranio nerve is cranio nerve 8, okay? So that's why they have problems with like hearing and stuff like that. And remember that this tumor, I mentioned this in the previous podcast, these tumors classically arise at the cerebellum point in angle, okay? They arise at the CP angle. In fact, they are the most common tumors that arise at the cerebellum point in angle, right? So basically, like it's sort of like a junction between the cerebellum and the ponds. Remember, the second most common tumor that arises at the CP angle is meningioma. Remember those associated with some homobodies on histology? And then the diagnostic testing again, because this is a brain, because this is a brain CNS problem, you make the diagnosis best with an MRI. Okay, next question. So, Port One Stain plus glaucoma, plus seizures, plus intellectual disability, plus tram, track, CT calcifications. I show you this picture of this beautiful baby with one side of his face red, okay? This is a sturgueber syndrome, okay? Very high to know that this is actually not a heritable disease. It's actually something that arises sporadically. And really, the thing that happens is it arises from a, I guess you can think of it as like an activating mutation in a gene known as GNAQ.

So, Giaz and Gatfri, and as in Nancy, as in Apple, Qiaz and quality, okay? So, it's an activating mutation. So, it's something that's sporadic. So, it's not something that's actually, it's like a somatic mutation, if you may. It's basically like an issue that arises in the development of like misoderm and I believe ectoderm. So, these cases, they tend to have like intellectual disability. If you do imaging of the brain, you see like tram track calcifications. Remember, yeah, so you see like tram track calcifications, you see they may have like some weird like like martial missions in the brain. And it's usually Ipsilateral to the port wine state, which is what we see grossly in this chat. So, next question, restless lexendra, right? So, you should not take your neurology shelf without knowing about restless lexendra, right? Like it's one of those things you can pretty much guarantee that you'll find on most neurology exams, even step two, step three, and even step one, right? So, restless lexendra, the classic presentation is it's almost always in a woman on tests, but it could be in a man, but classically it's in a woman, and they'll tell you that she has trouble sleeping, right? Because she feels like something moving in her leg or something weird. Basically, like some weird lex sensation that's worsened when the patient goes to bed.

Think about restless lexendra, and the demographic again, classically it's in women, and the associated CBC anomaly is actually has a weird association with iron deficiency andemia. So, one thing you actually doing the workup of restless lexendra is actually to get a 13 level, just to make sure that you don't have some kind of iron deficiency andemia gain going. And then in terms of treatment, you classically treat this with dopamine agonist, right? So, you can use drugs like Prami Pexo, or Ropinerol. So, Prami Pexo and Ropinerol are dopamine receptor agonists. Alternatively, you can actually give a babitri, there's one known as Primi Done, and believe it or not, that is fairly commonly tested. Primi Done is a babitri, that can be used to treat restless lexendra. Now, final question, couple tonal syndrome, right? So, the classic presentation is the describe a patient that has trouble with their first three and a half digits, right? So, like the thumb, the index finger, the middle finger, and the one half of the ring finger, okay? And I'll tell you that the lost sensation on the powermar aspect of the three and a half digits. Remember, that is median nerve territory. Remember, the radio nerve actually does the, I guess we can call it the dorsum, right? So, like basically like the non-palm part of your hand, right? So, the dorsum of the hand for the first three and a half digits is done by radio nerve.

So, if a person has couple tonal syndrome, which is a median nerve pausing, they won't have any issues with those, okay? So, they won't keep that in mind. And then, they may tell you that they have like atrophy of the thinner muscles, right? So, thinner refers to your thumb. So, if you have thinner muscle atrophy, think about couple tonal syndrome, okay? And the classic patient population, right? So, the thing is, I mean, couple tonal can arise in people that like sort of overuse their hands, right? So, if you're like a person that furiously types on a keyboard all the time, you can get couple tonal with that. But couple tonal can actually be a presentation of rheumatoid arthritis, right? It can actually be a presentation of pregnancy, right? And it can also be a presentation of hypothyroidism. So, basically, anything that causes a dima, like generalize the dima, right? That can trigger, that can sort of trigger couple tonal syndromes. Now, the physical examineovers that you can use to elicit symptoms, there is actually a nice no-monic that I use to remember these. So, there's two, right? So, there is a t-nail sign and then there is a phalian sign. So, remember the t-nail for t-napping. So, if you sort of tap over the couple tonal, you elicit symptoms. And then the other one is the phalian sign. Think of phalian like flexing, okay? So, the phalian sign is when you flex the wrists bilaterally. Tell the patient to hold that position for like 60 seconds.

If you reproduce their couple tonal symptoms like the pain and pasteges in a million nerve distribution, that confirms your diagnosis. And really, it's something that's for the most part diagnosed that clinically. And it is super, super, super high yield to know the stepwise management of couple tonal syndrome. So, the first thing you do is a wrist split, okay? You basically keep the hand in a neutral position, okay? If that doesn't work, your next step on exams is to jump to an end set, right? So, like ibuprofen, naproxen, stuff like that. If an end set does not work, the next thing you want to jump to on test is to inject steroids into the couple tonal, okay? Now, if that does not work, then you go for the nuclear option. The nuclear option is to cut the couple tonal, okay? So, high yield to know this. wrist split for starters, that doesn't work end sets, that doesn't work inject steroids into the couple tonal, that doesn't work per se to cut in the couple tonal. But the thing is, before you chop up a person's couple tonal, you most certainly want to do a nerve conduction study. You just want to confirm that you have a median neuropathy before cutting that couple tonal. So, very high yield to know those. And that is where I'm going to stop. I really hope you get something out of this. I will come up with our next episode, hopefully something this weekend. So, have a great rest of the day and God bless. I'll see you next time.

Fever, headache, and focal neurological deficits (Note: Nuchal rigidity may be absent).

Albuminocytologic dissociation (high protein, normal/low WBC count).

Isoniazid.

GEL (Group B Strep, E. coli, Listeria).

Third-generation cephalosporins like Cefotaxime or Ceftriaxone (Note: Avoid Cephataxine due to risk of intrahepatocolitis).

Vestibular schwannoma (associated with NF2).

Tinel's sign (tapping over the median nerve) and Phalen's maneuver (full wrist flexion).

1. Wrist splinting (neutral position); 2. NSAI Ds/Oral anti-inflammatories; 3. Local steroid injection; 4. Surgical decompression (if refractory).

Bacterial: High WBC count with neutrophil predominance, low glucose. Viral: Normal opening pressure, mild elevation of lymphocytes, normal/near-normal glucose.

To prevent the RIG from binding up the vaccine antigens, ensuring the patient can mount a proper immune response to the vaccine.

It is caused by an activating mutation in the GNAQ gene; imaging typically shows tram track calcifications.

Isoniazid (INH); Supplementation prevents peripheral neuropathy because INH depletes Vitamin B6, which is needed for the conversion of glutamate to GABA.

Tinel's sign (tapping over the median nerve) and Phalen's maneuver (full wrist flexion).

1. Wrist splinting (neutral position); 2. NSAI Ds/Oral anti-inflammatories; 3. Local steroid injection; 4. Surgical decompression (if refractory).

Bacterial: High WBC count with neutrophil predominance, low glucose. Viral: Normal opening pressure, mild elevation of lymphocytes, normal/near-normal glucose.

To prevent the RIG from binding up the vaccine antigens, ensuring the patient can mount a proper immune response to the vaccine.

It is caused by an activating mutation in the GNAQ gene; imaging typically shows tram track calcifications.

Isoniazid (INH); Supplementation prevents peripheral neuropathy because INH depletes Vitamin B6, which is needed for the conversion of glutamate to GABA.