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Tuberculous Meningitis

by Carlo Raj, MD
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    00:01 We’re moving on to tuberculous meningitis.

    00:03 So tuberculosis.

    00:05 And so when you say tuberculosis meningitis, keep in mind that granted, it is bacterial.

    00:09 However -- However, I need you to keep this separate from the other bacterial causes that I’d walk you through based on the age groups Are you with me? Remember that table that I gave you where it was predisposing factors, but it was age groups, right? And I gave you specifically those bacteria.

    00:27 You’ll notice that in that second column, that there is no tuberculosis there because you’re keeping it separate.

    00:34 If you do that for me clinically, you’ll be in good shape.

    00:37 Now, the onset here will be insidious.

    00:40 Your typical symptoms that you would expect, photophobia, headaches, so on and so forth.

    00:44 And here, it causes a? Please focus on basilar meningitis.

    00:51 In other words, secondary angiitis could also be possible because of its location.

    00:58 Is that clear? The most important point in this slide, in this section, is going to be that last statement of where it’s affecting your meninges.

    01:09 And what you’re finding here on your CT, now granted, in your particular point in education that by looking at the CT, you would need to have proper history so that you would then identify what you find in that arrow as being the actual pathology.

    01:27 Let’s continue.

    01:28 Complications: They may result in hydrocephalus, but for the most part, whenever you have meningitis, at some point in time, you’re going to scar.

    01:39 You could scar the arachnoid granulation.

    01:42 Picture that for me.

    01:43 Close your eyes.

    01:44 Are you with me? Arachnoid granulation, where are you? Subarachnoid space and this will be the drainage point of your cerebrospinal fluid.

    01:53 What if you scar them? If you scar them and if you’re not familiar with the concept of hydrocephalus, this will a communicating, nonobstructive type of hydrocephalus.

    02:04 What did I say? Communicating.

    02:06 Why? Don’t worry. It’s to come.

    02:11 And it’s nonobstructive.

    02:12 Why? Also an explanation that I’ll give to you when the time is right.

    02:18 Stroke: what happened here? Remember, you could have blood vessels that are affected, interesting.

    02:26 And with stroke, what does that mean to you? It means that there is a lack of blood supply to whatever part of the brain.

    02:33 So if you know for a fact that tuberculosis or tuberculous meningitis could affect the basilar part of your brain, and you could then affect adjacent and result in angiitis, specifically causing obliterative endarteritis.

    02:46 What does that mean to you? It means obliteration of the endartery to that particular tissue or organ.

    02:52 Uh-oh.

    02:53 This time, I have— The end organ is your brain.

    02:57 You got a stroke.

    02:58 Clear? Here, we’re going to evaluate the cerebrospinal fluid for tuberculosis or tuberculous meningitis.

    03:06 Keep this separate from all the others because the findings here are going to be a little bit different.

    03:11 Here, predominantly, your WBC would be lymphocytes.

    03:14 When else would you find lymphocyte perhaps? Viruses.

    03:18 Interesting.

    03:19 So you’ll find tuberculosis being a mix between bacterial and viruses.

    03:23 Do that for me, you’ll be in good shape.

    03:26 In bacterial, what kind of WBC would you expect to find? Good.

    03:30 Neutrophils.

    03:32 RBCs, none.

    03:35 When do we see RBCs in cerebrospinal fluid? Oh yeah, encephalitis or maybe brain abscesses.

    03:42 Meaning to say parenchyma involvement.

    03:47 Look at this.

    03:48 Glucose, concept? This is mycobacteria.

    03:52 There you go.

    03:53 So what is it going to do with glucose? Consume it.

    03:57 Interesting.

    03:58 So I told you with tuberculosis meningitis, it’s a hybrid in terms of CSF findings between your viruses, lymphocytes, bacterial with neutrophils.

    04:10 Here, with tuberculosis, you’d find lymphocytes.

    04:13 Bacterial, glucose, you’d expect that to be decreased as you see here.

    04:17 In viruses, glucose will be relatively normal.

    04:21 Protein on the higher side.

    04:23 And that’s pretty much what you see with any type of meningitis.

    04:27 But particularly higher with bacterial and here, we have tuberculous.

    04:32 Are we clear? So in order for you to understand this slide, I would recommend that you understand your findings for bacterial and viral meningitis first, then take a look at your CSF findings for tuberculous.

    04:46 Let’s continue.

    04:48 Let’s take a look at management of your tuberculous meningitis.

    04:51 This obviously keeps advancing, but at this point, at least know the basics.

    04:54 RIPE, R-I-P-E, and R referring to rifampin.

    04:59 I, INH.

    05:00 P, pyrazinamide, E, ethambutol.

    05:02 And of course, you know about INH in all its glory in terms of causing sideroblastic anemia, right? Maybe consider moxifloxacin.

    05:14 Steroids.

    05:15 Obviously if you’re talking about taking care of the inflammation.

    05:18 And you want to think about giving more or less a drainage, right? So you have your ventriculostomy for hydrocephalus.

    05:27 Always a possibility, isn’t it? Surgical decompression if required.

    05:31 For sure, because of that increased intracranial pressure.

    05:34 Management of tuberculous meningitis.

    05:36 In greater detail, know it well, know it well.


    About the Lecture

    The lecture Tuberculous Meningitis by Carlo Raj, MD is from the course CNS Infection—Clinical Neurology.


    Included Quiz Questions

    1. Basal region
    2. Corpus callosum
    3. Frontal cortex
    4. Pituitary gland
    5. Occipital cortex
    1. Steroids
    2. Surgical decompression
    3. Rifampicin
    4. Moxifloxacin
    5. Ventriculostomy
    1. Hydrocephalus
    2. Subarachnoid hemorrhage
    3. Meningioma
    4. Pseudocyst
    5. Calcification
    1. Due to vasculitis of the end arteries to the brain.
    2. Due to colonies of mycobacteria obstructing the end arteries of the brain.
    3. Due to rupture of the end arteries of the brain.
    4. Due to increase in neutrophils causing obstruction to the end arteries of the brain.
    5. Due to atherosclerosis of the end arteries of the brain.

    Author of lecture Tuberculous Meningitis

     Carlo Raj, MD

    Carlo Raj, MD


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