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Surgical Neurology International, and SI Digital Innovations and Learning in association with the Sub-Saharan African Neurosurgeons. Our pleased sponsor of the Sub-Saharan
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International Neurosurgery Grand Rounds
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held on the first Sunday of each month.
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This third Sub-Saharan African International Neurosurgery Grand Rounds is entitled Global Solutions to Clinical Challenges in Neurosurgery.
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Their discussions from Africa, Argentina, France, Persia, and the USA Our leaders are Estrada Bernard and James Osmond.
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This speaker will present a comprehensive review of the diagnosis and management of Tuberculoma of the brain
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on his experience in Kenya.
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Lecture and discussion is 40 minutes. It will be given by Professor Nim, JM. Wagwambi
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with multiple degrees from UK medical schools and universities, he's a professor of surgery at the School of Medicine and Kenyatta University in Nairobi, Kenya. His email contact is listed. He's
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formerly head of neurosurgery and professor of surgery at the University of Nairobi in
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Kenyatta National Hospital Campus and research registrar of the National Hospital for Neurology.
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and neurosurgery at Queen Square in London, England.
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So the discussion will actually be on tobacco lomas and not hide it, it's a very long topic and it will take a bit of time. And what I'm going to present is a case we managed with my team and the
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team which we managed with is Dr. Kanja, Dr. Kanja was the
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primary surgeon. Dr. Anjiro was the assistant surgeon. Dr. Ojimbo was the radiologist who assisted us in making the diagnosis and Dr. Okema was the pathologist who did the pathological diagnosis
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for us. Now we present a case of the glomer of the brain managed in Arabic Kenya. We review the role of surgery in the management of the branch of the glomers as seen in low and middle-income
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countries. We review the pattern of to Oklahoma's in Kenya, and maybe we'll touch a bit on the rest of the world. Now this is the case summary. 54 year old female, she's diabetic, which may have
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had a role to play in the diagnosis. She's a widow, para five, para zero. She presented with history of headache and grandma fits for a period of nine months, she had been put on nine to
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convulsions. Neurological examination shows a stable GCS was 15 over 15. And the only thing which you could detect was the pandoscopy short population. There were no, no lateralizing signs. Our
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clinical impression then was a special cappine lesion. She was referred to, she had been referred to us. Now at the area where she had been referred, a CT scan had been done. And the CT scan was,
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as happens in many
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areas where we've come from on this part of my country, the CT scan sometimes is done without contrast. And sometimes this is for financial reasons, because if it's done with contrast, then you're
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charged a bit higher. But sometimes when they do the CT scan, if they see something and they feel that this patient needs a referral, then they'll do a CT scan and they'll refer. And then the
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neurosurgeons or the managing physicians will decide what furthermore investigations need to be done. So this was the CT scan, it shows them at the referral hospital, which showed this part of the
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time of hypodensities, without calcifications, or hemorrhage probably bilateral frontal lobe vasogenic edema. The ventricles in these CT scans were normal, midburn and brain stem cells were normal.
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The differentials then were that this could have been high-grade leoma, or probably an infective process or probably metastatic lesions. So then she was referred to our unit. And when she came to
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our unit, then we proceeded to perform an MRI and these are the images which we did on the MRI. You can see here I've shown you the images on the left-hand side is T1 weighted image and then the
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right-hand side you have T2, T1 weighted image with contrast. So in the T1 weighted image, you have a large left frontal convexity, mixed signal lesion is seen. It is largely hypo-intense
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on T1 weighted pressure effects on the epsilon frontal cone You can observe that, and there is midline shift to the right, and that
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will bring a point as to why we made a decision to go ahead and do surgery. Now when we give contrast, then what was obvious was the left-crescentic shaft convex decision involving the Dura with
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ring enhancement, and very, very large surrounding pathogenic edema, and
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of course enhancement, you can see the Dura enhancements which you see on that And the other image, which here with MRI, we did in the T2 weighted and flare, there's hyperintense on T2 weighted
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and flare with extensive estrogenic edema. And in the diffusuated imaging with gradient, there was no restriction on diffusuated imaging and no blooming on gradient.
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So we, and then these are just the images which I've already explained to you. You can see the lesion, the main lesion is the one at the extreme periphery, which if you look at these images, the
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extreme periphery, that's where the lesion is and then what you see on the other sides are the associated vasogenic edema.
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Again, that's just to really emphasize those points. So we proceeded because of this mass effect, close mass effect, we proceeded to subject. We,
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at the time of going to surgery,
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Tuvacloma was really not very much in our mind, but it was one of the differentials, but we thought that probably this may be metastatic lesion
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or a high-grade glomer.
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Now, this is just a summary of the MRI and CT findings which I've already explained, and the conclusion was adding enhancing cryo-centric mass in the left frontal convexity with extensive prolesial
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edema and mass effect, and differentials which you are discussed with a new radiologist whether this could be an effective process or so it could be a cerebral metastasis or a high-grade glomer. So,
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this is the approach which we used
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and the patient was taken to theater and surgery was done the conventional way.
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Now, this is the patient position for surgery on the top left hand side, on
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that left hand side bottom, dissipation after the surgery. bone flappers already been replaced. Now, on the middle slide is what was seen. When we entered, what was found was that there was a
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lesion which was extra exo, it was not spreading into the brain, but it was compressing the brain and very, very much attached to the dura. And if you look at this slide on the right hand side,
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that is the dura with the lesion there attached to, and we actually could scrape it. And then on the left hand side, that is the lesion now, which was nitty gritty and could be dissected out, but
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not invading the brain at all. And there was some cascading material which was encountered during the surgery. So in fact, after doing the surgery, the impression was that this was an effective
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process. And because we do see these tuberculosis in our area, this was most likely tuberculosis, that was our clinical impression. And these sufficient that is just immediately left aside for it.
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She went home six days following surgery, and we started her on anti-TB therapy empirically, empirical why we waited for the pathologists to give us their report. Now, the pathologists dealt with
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this, I've discussed this with them, and unfortunately, they could not be with us today, but as you can look at these slides, the top slides, you see the granulomas consisting of lymphocytes,
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fibrosis, epithelial cells, lung-hans, gensils, and lung-hans ventricular gensils. And on the lower side, again, you see the multinucleate gensils of the necklace type.
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And in this, this is just a high magnification, which is showing those granuloma formation in that slide. We did a zen state, the zenissen stain, which was positive for acid, as alcohol, fast
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baciline So after this, and these are the tests which will come only.
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do in our setup, we don't do the polymerase PCR, we don't do that, it's not yet affordable to our patients, it's quite expensive.
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So the diagnosis then was a brain to a kiloma and the patient was put on anti-TB therapy in the conventional way. Once we make these diagnosis as surgeons in our federal hospitals, then we have a
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team which now takes over and
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gives the patient further management for TB. So it's not as we do it, but we have to be conversant with what usually needs to be done. And because we were not sure that this was to a kiloma, this
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patient before surgery, this patient was not put on anti-TB therapy before surgery. This was started after surgery.
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If there are any questions, I could take the questions before we go to the discussion part.
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Did you ever have an explanation for the decreased density in both frontal lobes, or do you think it was a demon spreading to both sides? Now, we think it was a demon spreading to both sides. That
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was our impression. And we think that this was a false, because there was a subfaulting humiliation. So we think that the subfaulting humiliation was the one which had made those features on the
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other side And
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then when
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you remove the tuberculosis, what was your option? How adherent was it to the peer? And were you able to - That's right. Okay. It was very, it was not a dryer, a dryer into the peer, but very
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adherent to the duel. Attached completed the duel and we had, in fact, we came out with the duel and we had to put a patch, duel patch to cover that gap I wondered if you might have had. The
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thickening of the pia to the extent that you could have, you could, you were able to separate it without disrupting the pia. I'm just curious about that and thinking in terms of what we might see
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with the meningioma, if you still have preservation of the arachnoid membrane But we were able to separate it from the pia surface without disruption, because it wasn't so adherent to the pia itself.
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I know you said it was very inherent to the doer Yes, and I think let me just confess that, you know, because I was not a primary sergeant and I may not be able to answer. I get your point, but I
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may not be able to answer that confidently And I guess I'll point.
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Yes, please, please. Okay, I'm sorry. I don't know this routine in your country. Do you do the skin test, PPT skin test over there routinely? The other question is that do they use BCG as a
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preventive on all the people, because in some countries, they give BCG vaccine to increase the immunity of the people They do it in Iran. They do it in most of the country, Mexico, everywhere,
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except US, that they don't give that BCG vaccine. So, is there anything that you do over there to prevent the tuberculosis? And also other question is that when you separate it from the Dura, the
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tuberculosis, did you have to replace the Dura with another artificial one or just you put it back. same thing it is.
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Okay, fine. Let me use of BCG is routine in my country. So we have very good immunization programs. And what I have found in over the years as we continue the discussion is that in spite of the
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use of the BCG, we still get patients who get TB and I've never been able to explain this. Now then the other one is the skin test. We do the skin test but usually we would do the skin test when,
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to recommend skin test, when we are very, very much in doubt. But in a case like this one where we have made a decision because of the mass effects to go ahead and do the surgery, we made no
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damage to recommend skin test. But then if, for example, some of the cases we are, there is no mass, much mass effects and we are considering making diagnosis and putting the patient on medical
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management without doing surgery, we may do tobacco and skin tests and then combine it with the other tests like ESR and blood works and if possible PCR and then if we are very positive then put a
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set of patient on anti-GP therapy and we commonly also do that especially in children who we encounter with CNS tuberculosis or small, and deep-seated where we feel that we have to, we can't even do
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a biopsy and we have to build a static patient on treatment for TB and sometimes those patients do improve. Thank you very much Dr. Nirmra, the point about the BCG, so administration if everybody
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is given the BCG that's going to give you a false positive on the PPD test right?
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Not necessarily, in fact, you'd be very surprised. Sometimes we do see this energy where the no patients have a
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BCG, and we do the skin test and still it's negative. But I must say that I
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can't confidently answer that question because I'm a sergeant. And I think the physicians or the pediatricians would be the ones who can give you a more confident answer on that matter. Okay, Ali
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had his hands. Yes, so yeah, we have a lot of patients from Mexico because they all have BCG over the routinely. And that is true. Those who have BCG, even myself, you know, have the BCG and
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TB positive on the skin test. And the routine, what the health department asks us, we do just the chest exchanges to show that There is no lesion and no need for the INH. put therapy or start any
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two-wheel tuberculosis therapy. And that is very true. There is a new blood test has come that they do it only in the hospitals and county when we have a doubt about the tuberculosis, which is very
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serious, sensitive, but still there are false negative cases. We had one case at UCLA that they missed it. And that is very true. And there are cases of refractory epilepsy,
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and we had a few cases coming from other countries to the US. and they were not reactive to any anti-TB therapy, and they had to be put on the current team. That is very true. There are refractory
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cases. And it's a major issue, even in the US. with the immigrant coming from certain countries, which is endemic over Thank you very much, Doctor, for your explanation.
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Thank you. So if I could continue, let me just review this subject, which we thought that we have done away with it, but nowadays it seems to be coming back. TB remains a major global problem in
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public health issue of considerable magnitude. In this instance, there's been recidance of TB, both in developing and developed countries. Several factors have been observed for this serious
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phenomenon The incidence, which as you see there in the US, is very low, nine cases, 500, 000 in developing countries like ours, it's 110, 000, 165, 100, 000. In my country, it's about
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almost 300 by 100, 000, 300, 100, 000, so it's quite a big, big problem. Now we did a review, and this is quite some time ago, because we see a lot of these tuberculosis, and we did a review
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of the cases where we, which we had managed and I know this is a bit of an and old paper, but I like coaching it because what we found is basically what we are seeing now, patients present with
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headache and seizures. And in many of our situations, we were able to, some of the patients had also systemic tuberculosis as well as chibaculoma. Now the mortality was quite high in our patients
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because of the fact that they tended to come late So quite a number of the patients, we lost quite a number of patients in those early years, 30 made a full full recovery. And this is the big
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problem which we get in our country because as much as if they come early, like this lady came early, then we can do the surgery and we get good results. But if they
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come later and this, as you see from the classification or the clinical classification of the disease, And let's say they are already - GCS is low, then many of them may not do so well.
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Now, we say, we still say this is a disease of low socioeconomic status, and we see most of the patients we see are young population. The patients who I saw in my study, most of them were below
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the age of 30 years. This later was in the 50s,
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but I remember she was diabetic, and I think probably diabetes may have played at all in the disease, HIV has increased the pool of patients with TB. Kenya is considered a high body nation due to
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the hyperreliance of TB where we are about 300
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per 100, 000 cases. Now this is a big problem we face when even us working in the wards, and when we work in the wards, we have to take precautions. And I have during my years at Kenya
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International Hospital, I had two of my residents who developed tuberculosis while they are. while they're working at the International Hospital. So we have usual to take those precautions, wear
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masks and take all the precautions as you work in the hospital, because it's quite easy to get the big TB while you're working in our situations. Now this is a map which is just showing you the
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prevalence of this condition. And they, as Dr. Said has said, they are seeing most cases now because of the migrant populations who are coming with these indices from the areas where it's endemic.
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But in our situations where it is endemic, these are cases we see quite regularly and we have to put them in the high list whenever we see patients presenting that way. And not all the cases do we
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operate with, because we're able sometimes to come up with a diagnosis that this could be TB and we have to make a decision to a patient needs surgery or not. This is just showing the predisposing
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factors. As you can see, the host plays a role. For example, if he's a suppressed, the environment plays a role, and the pathogen also plays a role. And if all these interact, then the
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condition becomes quite heavy.
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Predisposing factors have mentioned them there. Now, to backless involvement of the central nervous system, an important serious type of extra-paramolar involvement does measure that approximately
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10 of all patients with TB have CNS involvement. The incidence of CNS TB is directly proportioned through prevalence of tuberculosis infection in the general population, and that's why we get it
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quite often in the developing countries, and it tends to occur in the younger age group, and especially in childhood. And most of
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the organisms, as you all are aware, is my go back, tell him to the closest. But we need to bear in mind that in HIV-infected patients, then there are other types of organisms, apart from
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macarboxylic tuberculosis, which I will also mention. The pathophysiology, we all know about the rich focus, and sometimes the rich focus and its location may not spread, the lesion may just
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remain there quite a cent. But then after some time, let's say the patient is immunosuppressed or gets into some situation where the lesion now flares up, then now it may spread. And the ones it
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spread, of course, which can spread to whichever areas.
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OK, that, as I said, some of these things, I don't want to dwell them on them very much, because most of you are quite conversant with them And this is just
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to sort of discuss this case as to - what is the way forward or what do we do with this test of TB. Now, in this slide, we're sharing to you the TB and where we play a role as neurosurgeons in my
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country in managing this patient. We do see quite a lot of tuberculosis manyitis and sometimes we are called upon to manage a patient who has developed hydrocephalus because of tuberculosis manyitis
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and the other aspects are managed by the neurologists and we are not called upon to go
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into it. So, tuberculosis as I read about tuberculosis manyitis will go through it as in this discussion as to what exactly should we do? Should we put a shunt? Should we keep on draining until
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the hydrocephalus settles down and what are the risks of inserting a baby shunt in a patient who has got tuberculosis manyitis, which is active? And then of course, now, percuminitis, away now
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you have the palin camo to the kilometers as I've said. It's not all cases of palencomotrylachlomas, which need sagel. And in
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many situations, especially in us in developing countries, we have to make a decision as to whether the patient needs sagel. What I have found over time is, if there's mass effect and the lesion
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is huge, big, then we need to do sagel. And the lesion which we removed from this patient was amongst the small ones In fact, I would probably call it the one, the TB, which usually goes just
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through the dura and within the near the calvaryum. And but usually the ones we see the tuberculosis, we see are quite large and there's no way they can be resolved just with
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the anti-TB therapy. So this one, the one we did to in this case, the one I've presented was very, very much like of a kilometer in plague. Again, this for the diagnostic purposes, then one
25:40
needs to go ahead and do surgery. And
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that CNS spinal TB, we see quite a lot of it in my country, but in my country, spinal TB, as neurosurgeons, it's usually managed by the orthopedic surgeons and we rarely do surgery unless we get
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tuberculosis of the other spine itself And we do see that not so often, but we do see that in the investigations then we are called upon to do surgery for that.
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Intercuminative acclumors are
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firm avascular sphelical granulomatous masses measuring about two, eight centimeters. They are well-limited from surrounding brain tissue, which is compressed around the lesion and shows the demand
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gliosis. The inside of these masses may contain necrotic areas composed of cashiest material,
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Ocationally sick and prevalent, which tobacco bacilla can be demonstrated. Intercranal tuberculosis can occur at any age. In developing countries, young adults and children are predominantly
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affected while in developed countries, they are more common in the older patients. The symptoms will be related to their location. It could be low grade fever, headache vomiting, seizures, and
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focal neurogeoid deficits and papillae demand. In fact, in terms of ecalomas are more common in children and may present with brainstem syndromes. Cerebellumus manifestation does multiple cranial
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nerve pulses. We do see quite a lot of brainstem tuberculosis. And sometimes we have to distinguish this brainstem tuberculosis from brainstem tumors.
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And nowadays with MRIs, it helps us a lot. But the judgment becomes very, very difficult because I've seen quite a number of cases one time. tuberculosis and which once you put the patient on
27:38
anti-tibethalopy, they do very well and then you feel happy that this patient has survived and it's not a malignant. And again, this is just empirical
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management where you're just making a decision and the patients end up doing well. But whichever way, even if it was a
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point in glioma, we rarely biopsy point in gliomas in our setup here
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Symptoms have already gone through the symptoms. Griding, there are two types of grading. There's the MRC grading, the Velori grading. And the grading may have a good bearing on power. What are
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the results you get when you manage these patients? As you can see, our patient was stage one. She was fully conscious. She was no paralysis. But you can sometimes find that you're getting
28:28
patients who are good to kids level of consciousness or they're deeply comatose as per the MRC classification. And I think many of the patients, especially the ones who did badly in the study,
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which we did in our review, almost 30 or 40 years ago, were the ones who did well were in stage one, the ones who didn't do so well were in stage two, and the ones who died were probably in stage
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three. Now, we have to remember that the mortality in these patients can be high when the patients present late. Now, this is
29:02
the Velora grading And on the right hand side, this is the modified one, which is very, it can help you especially if you want to do a study on the cases because then you will get results which can
29:14
be reproduced or they can be explained. For example, if grade one, the G patients is GCS 15, nonological deficits like our patient, for example. And then grade two, GCS 15 with neurological
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deficits. And then grade three, now the patient is going GCs 9 to 14 and grade 4, the patient is now ready. a body-bound patient where you may not get much good outcome after the management. The
29:42
imaging studies, we have gone through that and I have taken you through the images which we did. And the imaging is very important because in many cases you can be able, if you have got good images,
29:55
to even decide that this could be to be a coma and you know, the one which doesn't need surgery and then continues to go ahead and manage it And sometimes in my country, sister psychosis is not a
30:09
problem, but in some countries where sister psychosis is a problem, then you have to bear that in mind when you see these granulomas that they could probably do due to sister psychosis. So
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especially in India and
30:24
I think my colleague in DLC, who I had a presentation like that last time. Now these are images we are sharing and really, I know this image is. or just like what you manage. That the role of
30:39
chest x-ray is very important because many patients like in our study, I think about almost 30 or 40 of the patients had systemic TB. So the chest x-ray, you must do a chest x-ray in these patients
30:52
to find out if there's active TB. I think our lady or patient may have had a chest x-ray or they didn't present it in this study. And this is just a chest x-ray which shows a patient who had merely
31:06
a TB. And of course, a patient who has merely a TB then is very likely to spread that merely TB to other areas.
31:14
Let's just a summary of how, what are the findings which you'll notice when you do the images.
31:22
Now we have also to bear in mind that
31:26
TB of the parenchimer may also be of the type of brain abscess, tuberculosis brain abscess These are two different types of conditions.
31:35
Chevakaloma presents with
31:40
the Guernuilomas while Chevakalasapsis actually presents just like the usual brain abscess. And developing countries, Chevakalasapsis have been reported about four to seven, about less than eight
31:50
percent in patients with CNS TB. And many times on my experience, it's almost impossible to say whether it's a Chevakalasapsis because a CT scan will just present like an abscess. And it's only
32:08
when you do the surgery that you realize that this could be a Chevakalasapsis. Now this, of course, is an image which of our characteristic features of a Chevakalapsis
32:20
and as I said, it's almost impossible from the images to know that this could be a Chevakalasapsis. And you just have to approach it as an abscess And then it turns out that this could be a
32:33
Chevakalapsis.
32:35
country where in my area where we're working, because we see a lot of TB, then always we have to bear in mind that this could be tuberculosis. And
32:46
then of course, in the
32:51
MRI, it has helped a lot because you can do MIS spectroscopy, which can help you now pinpoint more that this could be infective lesion rather than amalignant lesion. And it helps a lot in decision
33:05
making.
33:09
Now, usually these are solitary, they're large, and the treatment is the same. We have to
33:16
do surgery, drain them, and management is just the way we manage the usual brain abscesses. But I mention this because so that you can be aware of this. It's not as common as tuberculosis in our
33:25
country, but we do see it and we have to be at that in mind. And this is where we're sharing features of tuberculosis, features of tuberculosis, macroscopic you can see, kick wall in a
33:39
tuberculosis, sustain wall,
33:43
and usually the perulent center. And then macroscopic, usually you may not see much waving with a culture from the
33:54
path which you remove from a tuberculosis, while from a tuberculosis, most times you can be able to make a good historical diagnosis chivacala subsets because, as I say, you can see it's only
34:07
about four. to eight percent of the cases of sinus involvement. They're not so common and I haven't managed to write a wrote a paper on brain abscesses, the brain abscesses which you did were
34:19
pyogenic and none of those cases were tuberculosis.
34:26
Now this is a situation of tuberculosis, tuberculosis which is rare and seen as dual best and sometimes I'm wondering whether this patient way presented was not to a coloma in plaque, mass forming
34:40
localized meningial processors and benign implant meningioma or meningiometostasis, it's commonly in the frontal or parietal lobes and it may be intermispheric and of course the treatment is the same,
34:52
you just have to, if there's mass effect you have to do surgery and you remove them.
34:58
Now the HIV is still a problem in our country and
35:05
the only advantage we have is that they're good drugs now. The availability of very good drugs so that the patients can be able to lead almost no more lives even if they're diagnosed to be HIV
35:17
positive. But it's still a big problem in my country and it's one of the big challenges which we face. And this is one of the reasons I think why the TB is reimaging because the fact that the
35:30
patients have immunosuppressed, then it has resulted in TB again becoming a big, big major problem. Now the patients who have
35:42
HIV positive, they type of tuberculosis, it is a bit different because they call what you call macobacterium, avium complex MSC, and where there's either macobacterium
35:56
avia or macobacterium intracellularly. So one has
35:59
to bear that in mind when you diagnose these patients and especially if sometimes maybe they may get TB resistant and we do see cases of TB resistant and it's very unfortunate because you find such
36:12
situations as well as you can do and many of those patients usually succumb to the illness. But we have to bear in mind the CNS involvement which may occur in about 20
36:32
of patients with AIDS Your diagnosis I've gone through it. What I would like here to mention is
36:37
we just talked about interdominal tobacco and skin test is helpful when it is positive. But it can be negative and in many of our situations which is sometimes negative. Now remember when it is
36:49
positive then you have to learn how to interpret it. So you have to interpret it so that it has to, because in many situations in our country it will be positive because patients have good
37:02
procedures. But if it is high-propositatives which I think is certain
37:08
10 millimeters, then we say that it is positive. Then
37:14
the question now, if it is negative, what do you do? Therefore, in many situations, you find it may not add much value to your management of that patients. And then of course, you have to bear
37:26
in mind as I've said, talked about ESR, the WBC total and differential. All this coming to mind when you're considering managing the patient conservatively, without doing surgery, which many
37:39
situations where there's no mass effect and we have to make a decision, whether it was that the patient or an anterior therapy or not, then we rely on this diagnosis. But again, as I may say, in
37:54
my setup, because it's a referral, most times we're working in a referral hospital, these are no decisions which we make. So these are decisions which are made by the senior physicians who manage
38:04
these conditions will come and do all those tests and make the decisions.
38:14
Now, the PCR test in my country is very expensive. It costs like 20, 000 finished shillings. That's about, let's say, about100,
38:31
200, so it's quite expensive, and a patient has to pay for them from their bucket So we rarely do it in my country, except in the, as for private patients.
38:44
Now management, again, as I said, management will leave it to the physicians, but as a surgeon, you need to be aware of how the patient is going to be put on the treatment, and the management
38:57
really is guided by the
39:00
WHO guidelines, you know, on the drugs which I use, which I've listed there, so this is how we, the management process, and usually we put this patient on treatment. for minimum 12 months or up
39:14
to 18 or 18 months.
39:18
But again, as I've said, this is done by a special team and not only physicians, but we have in our country a special team which handles TB cases. So they're the ones who handle the infectious
39:29
disease, going to infectious disease control units. They're the ones who handle
39:35
and they follow up these cases. And that is of course, it's very clear because these are drugs which we are not keen that people should play around with them just in case patients develop resistance
39:46
to these drugs. So that's why they're handled by teams which have been designated that role of doing that.
39:56
These treatment regimens are, I think what is important here for is as I've said that this is long-term management and usually with BSPT, I know people talk about three months, six months, but
40:08
usually we give about 12 months to 18 months of anti-tubularity. these patients.
40:15
I would mention about that. Now, the role of corticosteroids. Now, this is one of controversy aspects on the treatment of trachylasminitis is the use of corticosteroids. The response to steroids
40:27
may be dramatic with rapid cladding of sensolia. It was believed that corticosteroids
40:32
had no place in managing rectalasminitis.
40:34
I mentioned this here so that you can bear in mind what happens, for example, in this situation where we call paradoxical worsening. Because in terms you have a patient who has got
40:45
tuberculasminitis and then after you have managed
40:50
to increase rectilasminitis, you find that he has developed a tuberculoma and because this is what we call paradoxical worsening. Now, when these patients who have been managed for
40:59
tuberculasminitis will then incidentally end up now to be found out that they've got tuberculoma. When they're put on steroids, the steroids may suppress those So, and that's one of the reasons. I
41:13
think in your surgery, we have to bear that in mind that steroids may play a major role in managing these cases. But I mentioned here that this is not tuberculosis management, this is not
41:28
tuberculosis management management. But now we mentioned the steroids, because patients with tuberculosis meningitis, we've been managed for tuberculosis meningitis steroids, may some type of
41:39
tuberculosis meningitis patients end up having developing
41:46
tuberculosis, maybe it was a solitary lesion, now it flares up. But then because of these steroids, these may suppress that stage of the illness.
41:55
Surgery, I've already talked about this, and I've already
42:00
mentioned about the role of surgery in tuberculosis, especially if there's mass effect I'd like to
42:11
dwell on ventricular peritoneal trans patients who are good. hydrocephalus and tuberculosis meningitis. Ideally, one may want just to see how best you could contain that hydrocephalus. But if one
42:21
finds that it's not possible to contain the
42:26
mesetrocephalus, one may opt to go inside to place a ventricular patient on a shunt. But you have to remember that because of the hypertension content of the CSF, then the blockage of this shunt is
42:36
very common. And this, I think, well, this one of the reasons why the
42:41
neurosurgeons really would like to see if that situation can be managed conservatively. And I've talked about that, the medical therapy for the shunt, both for the
42:54
hydrocephalus and all that.
42:57
And of course, there's a situation where sometimes theoretically it's been said that you may disseminate the TB by placing a ventricular peritoneal shunt I have never encountered that and we are
43:10
blessed to be patient soon.
43:18
in patients with tobacco, blood syngetis, who have developed a risk of less, but I've never encountered dissemination of the TB interperitoneal eso, but I have encountered the chance blocking
43:23
quite often, and you need them to go back and revise it many times.
43:31
Indications of surgery, we have talked about that. And remember, patients who are grade one
43:38
and two, they do very well, grade three four. They don't do so well, and you have to make a decision as to whether surgery will be beneficial in those patients or not.
43:48
If surgery is done early and in the early in the
43:53
patients, then the outlook is quite good. Like as you have seen, this patient did quite well. We did, but again, as I've said, from the paper which we published, we lost quite about 30 of the
44:05
patients who are losing, who had children, but one of the reasons, of course, Is that what presenting let? and a patient's presenting lead is quite common in our situation, in our country, and
44:17
there are a lot of constraints, factors which make our patients come lead.
44:24
My name is Dr. Baklomas. I've talked about them. I would like here to mention about the role of biopsy for tuberculosis. If, for example, you find that there's a little indication for doing the
44:37
compressive surgery, then one may opt to do biops of the lesion, but in areas where this situation is endemic, we find that sometimes we are guided by the clinical judgment, and we may not even
44:50
bother doing the biopsy and just start the patient on anti-TB therapy. So, in conclusion, tuberculosis is re-imaging as a major public health problem worldwide. They imagine so of multi drug
45:03
resistance and interaction between TB and HIV infection and migration from TB-endemic developed countries are responsible for this surge. Emphasis should be placed on effective methods of TB control.
45:19
In our country, in developing countries, we have very, very effective methods of TB control and these are taken very seriously. All our children are immunized against TB at before the age of nine
45:33
months, at around six months or nine months, they're given BCG. But I noticed in developed countries, this is no longer done. But in spite of all this, because of the HIV and all those
45:48
situations, then we are still having a big, big challenge managing these conditions and these conditions are going to be with us for some time. I think I've come to
45:59
the this is my declaration and
46:04
there are no financial benefits and patients have given us the consent to discuss this case. Thank you.
46:13
Thank you, Nim, for the thorough
46:15
coverage of TB and the CNS. I wonder if you might comment about
46:24
using the CSF protein in your algorithm for placing a ventricular peritoneal shunt in cases of TB meningitis. Do you have a certain threshold before which you would use an external ventricular drain?
46:44
How do you use the CSF protein in those circumstances?
46:51
We don't usually use the CSF protein, so we don't routinely do that. Most of the patients, we just manage them.
47:02
Thank you. Dr. Do has his hand raised. Elvin, do you have a comment, a question? Yeah, thank you so much, Professor.
47:12
I was closely following your prison. And it is almost like the same thing that we do in Liberia. But the only challenge is for almost here regarding the management is that most often there is this
47:27
based understanding between the neurosurgery unit and because in labor, we do not have a neurologist. So there is this based understanding between the neurosurgery unit and internal medicine At
47:40
times some of these patients come with suspicion of TB of this pine, all right? And once they diagnosed, once it is, the
47:50
presumptive diagnosis is made,
47:55
we usually refer them to internal medicine. And you know, internal medicine, they have lot of things dealing with those patients will be delaying and when they come back to us, we do the CBC, we
48:08
do the complete blood count, We do the serative protein. to
48:15
baseline investigations to look for signs of infection. But most often - and then there is a particular unit responsible for the medication. And there, whenever they go there, there will be a lot
48:34
of delays. I don't know how is it - how is the delay being worked out at your center professor? That's question one. And then,
48:46
professor, regarding TB of the spine. I overheard you saying the orthopedic. So because we have done a couple of cases in Liberia with
48:58
the help of visiting neurosurgeons, spinal instrumentation surgery with suspected cases of TB
49:08
I mean, we refuse.
49:12
So what do you think of that? Thank you so much.
49:18
Okay, thank you, thank you. And let me start, let me answer your last question first. As I said, the, you know, the TB of the spine, the one which we do the surgery is one where the spinal
49:31
cord is involved and the patient presents with weakness, neurological deficits, and we do an MRI. And nowadays it's really very, very helpful because with an MRI we can be able to diagnose
49:44
tuberculosis, tuberculosis, very, very confidently. And then we go ahead and do surgery. Now remember now with TB of the spine, you can also get the situation you have, TB, other
49:56
cognitiveities where patients, almost presents almost the same. And now when we do all those investigations, we don't see anything which we can go in and help the patient. So that in that stage we
50:09
just have to manage physicians manage those patients. Then now we have the review of the spinal column itself, where now the patient represents with pathological fractures or collapses. Now, in
50:24
those situations, most of the patients who present with TB or the spinal column, we manage conservatively. We don't do surgery in those patients. And really, the results of conservative managers,
50:37
which are very good. And there are several reasons why we do that is because we don't, if we go in, then we can make the TB spread. So usually, manage them conservatively with bed rest, et
50:50
cetera, and they do quite well. I haven't, and as I've said, because it's not the area I handle
51:01
routinely, I don't want to give a very confident reply. But over the past years, over the past years. I never did instrumentation for TB spine or the pastures. So unless the times have changed
51:19
now, you get a good point. So times may have changed, but in the early years, we never used to do instrumentation for TB of the spine. For fear, again, as I said, of causing a spread and TB
51:35
is in our country is a very debilitating condition It kills many patients, and then one has to be very cautious so that you
51:47
don't subject this patient to do deterioration of the clinical condition. So that's the first question. Now, the other one which you had asked was, how would we manage the medical, the
52:01
condition, whether the patient has got this clinical condition? As I
52:08
said, that's traditionally case is very different. because we have a team which handles TB cases. So in each hospital, you'll have the teaching hospitals. There'll be an expert who is an expert
52:22
on infectious diseases. Now, usually in the peripheral hospitals, in the smaller hospitals, usually they'll refer to the big centers because this is a national problem. They'll be got the patient,
52:36
the big centers where the patient is reviewed and then put on treatment and they'll refer back to the small peripheral hospitals. And because we have quite a number of physicians, we haven't had
52:49
that problem at all. And as I said, the role which as neurosigens we play in management of these conditions is really on the complications. We don't play any role in managing the TB itself know,
53:05
and
53:07
I think for that reason, it's It's why we don't feel fester frustrations with your physics.
53:17
I hope I answered your question.
53:21
I think there, Ali and Professor Kaba have a question. Yes sir, if you don't mind, thank you very much for such a nice review. The type of the meniré TB, which happens if there's muscle sitting
53:35
on the body, especially on the brain, it affects the sixth cranial nerve. It's one of the things typical, which happens with the meniré TB The other point is that there is a test name, acid-fast
53:49
staining that we use to do on the sputum of the suspicious patient and the CSF. So that's another own technique, which is not 100 percent, but it's very effective in making the diagnosis of the
54:02
tuberculosis. Thank you very much, great review, sir I think we still do sputum analysis in my country and it's also almost routine. But again, as I said, it's not us who do it. It's done by
54:18
the physicians. Thank you.
54:23
Professor Kava?
54:26
Yeah, more than a question is a contribution. My point here is for 25 years, I have never had the opportunity to operate on any two-bed clumas in the brain here in Ghana. But yes, I performed a
54:41
lot on pod disease And in fact, I started operating on pod disease in Ghana and I'm happy to inform to side with Professor Dard. At the beginning, in the last 10 to 15 years, the first 10 to 15
54:57
years, we never, never had to put instrumentation in pod disease. And they do well. And most of them were thoracic. And most of them we did the trans-toracic approach and lateral approach to the
55:10
thoracic region However, listen to it.
55:14
I don't know for some reason. I'm here to find out why we decided that. Because of the level of destruction of the vertebra bodies, we have decided to push screws on a couple of them. Of course,
55:28
first, we're treating the TB, we're using the protocol, and then before we do the surgeries. But I'm still wondering if it is at the thoracic level, whether we should push screws or not.
55:40
Thoracic level, I had to do that But lumbar level, yes, I do think that they will benefit. Because the thoracic level, you've got the cage, and
55:49
I mean, the thoracic cage, and it can help. But lumbar level, I think that probably does where we put the screws to benefit, yeah.
56:02
Thank you. I think they, as I said, because I don't handle these guesses, so the answer which I'll give you will not be an absolute answer. The TB is handled by the orthopedic sergeants. And I
56:17
don't know whether now they're doing instrumentation or not. I really will have to get, I'll discuss it with them. I get a feedback from them. But we are called to do the surgery for spinal TB.
56:29
And we do maybe,
56:32
I remember maybe we'll do about three or four cases. But remember where I was working previously was a major referral hospital. So we're getting cases from all over the country
56:48
Alvin, did you want to make some comments?
56:55
Professor, I'll wait for the professor, Professor Samuel, I think he wants to talk. I'll wait. Yes.
57:03
Oh, thank you.
57:06
I just wanted to comment for an excellent lecture. I experience here is quite similar in a way. We see a lot of stability problem in Nigeria But the ones that are rich in the research course are
57:21
mostly spine. Occasionally, very occasionally, we see tuberculosis in the brain. We have one cut out once, in fact, where the diagnosis wasn't suspected. And then surgery was done well waiting
57:37
for the histology report, especially in developed many dietists, developed lots of many dietists. Unfortunately, despite intervention with drugs, we didn't save the life of the patient That was a
57:48
lesson, that once we suspect we will even commence. anti-tobaculose treatment while waiting for the histology information. Now we - Genex part, of course, has come here to help - has seen the
58:03
diagnosis. Also, we have had no questions. We are Bella's
58:11
concentric sclerosis, which is a variant of multiple sclerosis, had mistaken for a TB or tuberculosis of the brain. It was only histology But eventually, they took correct diagnosis. So we have
58:26
to be aware of it. Around the differential diagnosis for TB brain.
58:34
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