Guillain-Barré Syndrome (GBS) is characterized by acute flaccid paralysis with symmetric ascending weakness, areflexia, and bilateral facial nerve involvement, typically following a preceding infection. The clinical diagnosis is supported by albuminocytological dissociation in CSF (elevated protein with normal cell count). Key features that suggest alternative diagnoses include asymmetry of weakness, fever at onset, sensory level, or CSF cell count exceeding 50 cells/cubic mm. The condition requires prompt recognition as it can progress to respiratory muscle involvement requiring mechanical ventilation, though most patients show significant recovery with supportive care and IVIG treatment.
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PG CLUB - Dr Bala SubrahmanayamAdded:
Uh-huh.
So then you open on the L.
desktop. Put the other file in.
Um slides on the movie though. You got Video video.
Rago and Babu sir.
Something can match view.
form.
Yeah.
Start video.
Okay.
We have to just inform him and we'll tell him.
So if you really seriously want to be in the in the meeting definitely we have to follow the rules and regul speech start.
>> Ohh.
>> Okay.
Among us will start is waiting.
>> Good evening.
Uh today uh we are having IAP uh PG club. So today is ETH. So as per the calendar it was on 27th and it happened to be in 28th. So even then we decided to have the EG club uh today and uh another thing is uh we are here with a heavy heart uh Dr. Sadi who is a senior pediatrician in from Kim's tandum who was just one year junior to me in SAT when we did PG so he left us untimely so uh anyway uh today uh the PG club is organized by AP calicate branch and uh uh a very eminent faculty uh professor Balis Bman sir who is the head of academics institute of advanced pediatrics Raa women and children's hospital Chennai and uh he was uh in uh child stress hospital before so sir is the faculty today an excellent uh clinician and a very So it is very much sought after faculty for clinical discussion uh and the case is being presented by Sutena and for JR3 from IMC calicate and uh uh the mentor is Dr. Arushi Proer from Calikat to u before that I would like to invite Dr. Nandagumar MK who is the president of AAP Kerala state uh to say a few words.
>> Good evening all respected mandas chairperson for PG club then today's speaker most respected Balumasa then Dr. Shahana Shaavas Dr. Priya today's Dr. Arishi Dr. Sudena and senior pediatricians and teachers Dr. Dr. Dr. PK Parvi Madam and other teachers and my dear students on this platform as most Dr. Mandas already mentioned we lost Dr. Tadik were very close friend and uh definitely this anti leaders and I pay homage to his the department of soul and another pediat also left us last week. So I pray the almighty to give the eternal peace for these departed souls and I really I because today we have a great teacher as Dr. Mandas already mentioned here a great teacher clinician and great orator what not we are very lucky to have Dr. Drumas today because the PGs you are very lucky to have a teacher like sir and uh sir is going to discuss a neurology case today and without wasting much time st will go to the uh teaching programs and I wish all the very best for this program happy learning thank you all >> uh minister you can uh thank you uh Dr. Moand Das and uh Dr. Kumar it's always a privilege uh to take part in any PG discussion that too if it is from Calat I would really enjoy because I have always seen for the last decade or so the standards that your medical college maintains in uh in terms of PG training and also I have been almost every year coming to your annual event and uh as much as the students learn I go back with lot of learning after attending that's how I respect the clinicians of the state of Kerala I am indeed thankful for the privilege today to take a PG session in fact uh uh in fact before the presentation Dr. Mandakumar Dr. Mas sent a message to me asking me whether I should inter the PG should interact with me. I replied back that I don't like match fixing when it comes to clinical discussion. I said I'll be open and uh I will be willing to learn from the students as well as from the uh senior teachers who are uh in this platform. So I told him that I wouldn't like to know anything about the case. So Dr. SA uh please be relaxed. Uh if you're from Caligate Medical College, I don't think you should worry only. I should worry because you will know such much more than what I know. So relax.
Present uh uh the case details. If there is anything I do not know, don't worry.
I can ask Mo, I can ask Nandakumar and I can ask Dr. Parvati, my good friend.
Okay? Anybody I can seek support. So don't worry. Please go ahead Dr. Da.
Thank you very much.
Presenting the case.
A 9-year-old boy coming from Canor informed his mother. History related.
The present complaints were pain both lower limbs since 2 months. Weakness of both lower limbs 2 months. History of present illness. Nine-year-old boy who was apparently normal did two months back when he suddenly developed pain uh severe pain over both lower legs. It initially started over the calves posterior respong with back pain. It was deep aching in nature. Parents described that the child cried on passive movement of the lower limbs. He was given some pain medication on that day from home.
Uh not consulted for the same.
Same day evening mother noticed that the child was not able to stand and bear weight on his foot. There was bucking of knee when he was trying to walk and he had difficulty getting up from sitting position and also to climb stairs. He also felt difficulty in gripping onto chapels. Mother observed that his lower limbs were cold to touch but there was no history of any numbness or excessive sweating on the knees. Next day morning he was unable to lift his leg off the bed. He required support for standing and walking and his father carried him to the hospital.
>> Please go ahead.
He was initially evaluated at a local hospital and treated symptomatically for pain and sent home. And the next day his weakness progressed and he was not able to get up from bed but able to lift his head off the couch. He was not able to turn in bed independently and subsequently he developed weakness of both upper limbs with inability to lift arms above the shoulder level. Though he was able to move hands and fingers and hold objects. Then he was referred to a hospital with these complaints. By that time he had severe pain over the back and buttocks on lifting the leg. He was able to appreciate touch and reconize old and cold ores at that time.
>> Please go ahead.
>> No history of any fever contact with conduct with children with the weakness.
No history of altered sensorium seizure or difficulty in speech. No history of any fatigability or dal variation of the weakness. Noise of bowel or bladder involvement. No history of neck flow, inner fatigue, cough, muffled voice or breathing difficulty on admission. No history of any visual disturbance.
Impaired sensation of smell. Abnormal eye movement, chewing difficulty, difficulty eye closure, deviation of angular mouth or during of saliva on admission. No nasal tone of voice or regurgitation of feet. And also no history of palpitation, abnormal sweating, flushing or giddiness on change in posture. No issue of any bite or intake of any canned food or any drugs.
As the weakness was rapidly progressing, child was admitted in our ICU and was given IV medication. On day two of admission, he developed shallow breathing. He was not able to move both upper limb. There was mild drooling of saliva from mouth and there was a deviation of angle of mouth to one side.
uh that time we he was mechanically ventilated and feed was given by a NG tube intravenous medication given for five consecutive days. After 12 days of mechanical ventilation child was extated and connected to oxygen support for 2 days followed by Roma. By that time he showed some improvement in weakness of both upper limb. He was able to move fingers and shoulder.
After a few days there was some movement of toes and child was able to drag leg in bed. He was discharged after 3 weeks of admission and kept under followup. At the time of discharge he was able to lift upper limb off the couch. There was weak hand grip was present. Breathing was normal. There was mild facial asymmetry. Was taking feeds orally without choking. He was unable to lift the lower limb off the couch and there was flicker of movements of toes at the time of discharge. Subsequent visit he was complaining of pain in both thighs and legs for which oral medication were given. There was improvement in upper limb movements but lower limb movements were the same. He was bedridden since last two months. Bow and bladder habits were normal. Parents used to carry him for daily needs and mother was doing passive movements of link limbs and no history of any bed sore or diaper rash.
Since longer limb weakness was persisting he was again admitted and given IV medication.
>> Complete the past history also then we'll discuss.
>> Okay sir. Past history. He had history of a minor fall after tripping over a plate two days before the symptom onset.
But there was no history of loss of consciousness, altered sensorium or vomiting following that. He had pain over both knees. He had history of sore throat 5 days prior to the onset of fitness which was associated with the running nose and cough. Sore throat subsided within one day and cough was persisting. History of fever with the cough four weeks prior to the onset of the symptoms but no history of loose tools.
Those history of cat scratched seven months back. He took vaccination against rabies for the same. No of similar weakness in the past. No of recent vaccination bite or recent travel.
No of contact with TB. No of fever, rash or joint pain and no of abdominal pain or photosensitivity.
>> Antiatal natal were uneven full. Am I right? Nothing specific.
>> Nothing special, sir.
>> You can skip it. Yeah. Next.
>> Development was appropriate for age. He studies in third standard. Good scholastic performance.
>> Okay.
>> Immunized for age. BCG BCG scar was present. Last vaccination at 5 years.
Pulsefolio immunization was taken in 5 years. Complete dose of post exposure profile as of diabetes was taken 7 months back.
>> Okay. Go ahead.
Dietary history uh exclusively breastfeeding six month significant he is getting adequate diet.
>> No sir.
>> Okay this yeah then family history no similar illness in the family. No stress in a child with weakness. U an elder sibling died at neonal date. Um cause was not suspecting card heart disease.
>> Okay. So economic status um lower middle class family according to modified KUS Swami scape insurance.
>> Okay. Excellent. Excellent history.
Please go back to the first slide.
Please go back to the first slide. Good good presentation. Very lucid data.
Very well done. Sida.
Okay. Now uh a few few suggestions for improvement. one you had said that uh he was apparently normal.
>> Yes sir.
>> What made you say that he was apparently normal?
>> Uh he was a 9-year-old boy who was uh as usually going to school normally and no history of any weakness prior to that and >> he was he was an abs. Yeah, you could have I mean it's always better if you had mentioned that uh he was walking to school, he was doing normal things and he was absolutely well in terms of growth and development.
>> Okay. He had no other symptoms. Am I right?
>> Yes sir.
>> And you expect a 9-year-old boy to do things like cycling. Was he doing it?
>> Yeah. Cycling.
>> You could have mentioned those things to make sure. But you have mentioned apparently norm I I still agree with you for making it short. It's okay. Now suppose you had seen this boy on day one with this story with this story that there is pain in the calves uh and posterior aspect of thigh back pain and child was crying on passive movement to the lower limb. What are the conditions you would have thought of?
Imagine you had they had come to you on that day itself.
>> Oh okay sir as they gave a history of um a fall minor fall 2 days prior to that history prior to the onset of this pain.
So uh initially they will suspect a mechanical pain because there is a fall but uh the pain is like a radiating type of pain like like there is back pain pain over the cal thigh and all. So uh >> so where do you think is the pain arising from? See a pain in the limbs can arise from the skin can arise from the soft tissue subcutaneous area or or in the muscle or inside the uh soft tissues in the bone or in the joints or it may be a referred pain. How would you distinguish all this and what do you think was the cause for the pain at this point of time?
>> All right here uh there is uh it is a deep uh deep aching type of pain with which increases on passive movement of the lower limbs. So uh mostly I would suspect uh nerve involvement or neurologic pain like that. Uh >> okay. So what other question you should have asked the mother to say that this is coming from only from the nerve.
>> Um uh whether there was any p tenderness like >> tenderness or swelling. I think you could have mentioned very well there itself that without any tenderness of the muscle or on palpation right >> okay it looks like a neurotic pain and uh at this point we do not know I don't think just ripping and falling and the child becoming completely normal immediately without a big jol to the back that fall is significant or not we can't say it doesn't look like it is significant.
Next >> please go to the next next slide.
>> Okay sir.
>> Yeah. Yeah. Here here you have very nicely described what has happened. You have mentioned that uh the child was not able to stand and bear weight. Buckling was there. He could not uh get up from sitting position. They also could not grip the choppers and the lower limbs are also cold to touch. Okay. Right. And next morning he was unable to lift the leg of the bed and he could not even stand or walk. Isn't it? So what has happened here between the time the night where he started having limp pains to this you know weakness severe weakness making him unable to walk or stand >> what has gone wrong from your description?
Uh initially it was only pain then there was rapid uh progressive weakness. Uh there was >> a type of weakness which is happening.
>> Yeah there is both proximal and dist weakness.
>> It started first proximal started first or dist started first.
>> Uh it was like first there will be buckling of knee was what mother noticed first? No no this boy had initially proximal weakness and then developed distal weakness or initially developed dist weakness and then went on to develop proximal weakness.
>> Initially it was dist weakness type uh there was >> excellent the first problem was only a dist weakness distally you had very clearly said that you could not bear his bear weight on the foot. Okay. Okay.
>> And of course it progressed and to the extent of not being able to even lift the leg of the bed, right?
>> Yes sir.
>> Okay. So it looks like it is an ascending paralysis. Am I right?
>> Yes sir. Ascending.
>> That's your conclusion. So initially pain then ascending paralysis involving both the lower lips. Next. Next slide.
Next slide.
Yeah.
Go ahead. Uh in this you had mentioned that he was evaluated okay and he he became he he was bedridden and is he developed weakness in the upper limbs and upper limbs the weakness was ascending or it was descending. on presentation uh he was only complaining of weakness of the um arms only fingers and fingers were normal like there was only proximal weakness on presentation.
So in the upper limb it it it he had proximal weakness later went on to develop >> this.
>> Okay then. Okay fine. He had severe pain over the back and buttock. Back means which region of the back?
>> Lower back lumbar region and >> lower back. Lower back. Lower back. Do you think that is significant story with this story?
>> Yes sir. can be radicular pain starting from the lower back radiate to >> radicular see here this boy has almost developed quadriperosis >> yes sir >> so he cannot have a lesion lower down no you are saying back >> yes sir >> okay I don't think that might be significant because it looks like the the whatever weakness that he had had progressed to involve the upper limbs >> upper limbs are involved why are you worried about pain in the lower spine or buttocks.
>> Okay.
>> Unless you you are thinking of multiple lesions, one lesion lower down in the spine and one leion upper uh in the upper region of the spine. Okay.
>> Right. And you had very nicely mentioned that he was able to appreciate touch and recognize hot and cold indicating that there was no sensory involvement. Am I right?
>> Yes.
>> Okay. Next. Next. Next.
Next slide please. Yeah. here you know uh I'm always reminded of one of the toughest examiners and my good friend there is one Dr. Subra from Bangalore >> okay >> he will always criticize too much of negative history too much of negative history >> and that's what is called negative exuberance you can't I mean you don't have to have a French index of differential diagnosis and mention all the diagnostic possibilities in the given case but having said that let me ask you uh history of fever contact to children with weak weakness what what made you ask that question. What condition you think of >> polomi to rule out polomi >> 2026 do you think it is put it as a first sentence that's why I noted it but you presented earlier I knew I'm going to catch you on this how common is polio in 2026 >> so I don't think highly highly uncommon this is what is called irrelevant history >> highly uncommon unless it is there you don't have to mention it is not there.
>> Okay.
>> Right. Polio is now non-existent. Okay.
>> Number two altered sensor seizures and difficulty in speech. Why?
>> Uh as is a child is with weakness. Uh it to roll out like it is not a lesion like there is no uh >> do you think this is lesion whatever this boy is having from the history?
Uh there is initially there was pain followed by >> no you please tell me whether this boy has got a he has got ascending paralysis. Do you think he has got a flaccid weakness or a weakness?
>> Flaxid weakness.
>> But did you mention about the tone from the history?
>> Uh tone >> but if you go back to the previous slide go back to the previous slide please go back. See you said he was bedridden.
If I were you, I would have mentioned what was the posture. How would that help you in distinguishing uh weakness and a flaccid weakness?
>> Uh if it's a uh flaxid weakness, the lower limbs will be abduct at the hip.
It will be abducted externally rotated.
>> Yeah. Yeah. So what is the posture of this child? What are the what are how are the lower limbs? How are the upper limbs? uh lower limb was like uh at the hip it was externally rotated and abducted and knee was mild mild.
>> Excellent.
>> Yeah. Go back to the next slide. Go back to the next slide.
Yeah. If that is so your history of altered sensorium, she has difficulty in speech.
>> Okay.
>> Off isn't it? Definitely altered sensorium. You're not thinking of cerebral leion in this boy.
>> Okay. Right.
>> Why did you ask for history of diural variation? Uh myastthenia.
>> Okay. Okay. Agreed. Agreed. Bowel and bladder indicating that autonomic nervous system is okay. Neck flop, ineffective cough, muffled noise or breathing indicating that this boy does not have any respiratory >> respiratory involved.
>> Okay. Agreed. Agreed. Agreed. Visual disturbance >> cranial pales sir.
>> Okay. impaired sensation of smell uh alactory.
alactory how many cases of alactory weakness you have seen in cases like this that's what I said irrelevant >> I don't mention that >> okay sir >> okay and at this age the boy won't be what is his age >> n years he even if he has got some sensation disturbance he won't be able to perceive it properly >> okay >> abnormal eye movements for what >> okola muscle paly >> okay agreed difficulty in chewing For what?
>> Uh fifth nerve RC.
>> Okay, this is what I said too much. You know, for every nerve you have given some symptom not but you instead of saying that you could have said positively that though he had severe weakness he had no involvement of the >> face, eyes or ears from symptomatic point of view. I think that would have been appropriate instead of giving so many points. Okay.
>> Palpitation you're rolling out autonomic distalism.
>> How common is bottism in this age group and >> rare? Rare in this age group.
>> Yeah. Okay. Fine. Our uncommon it is okay. Any drugs? Okay. Please go to the next slide.
Yeah. Then you had given the story that he was admitted in ICU, given IV medication and he developed shallow breathing indicating respiratory embarrassment. He is ventilated.
Okay. Medications are given, extrated.
He did show improvement in both the upper limbs. Able to move fing fingers and shoulder. Go to the next slide.
>> Go to the next slide.
some moment of that term. Okay. Now at this point when he was discharged was he able to walk?
>> No sir, he was not able to walk.
>> So what was the neurological status at that point of time? What had improved?
What had not improved?
>> At the time of discharge, he was able to lift the upper limb of the couch. There was weak hand grip uh >> and but facial asymmetry was there and bulbar was not there but uh he was unable to lift the lower limb off the couch and was only a flicker of movements of toes.
>> So he did have paraparosis though upper limbs appeared to >> improve >> improved marginally. How much was the improvement in the upper limb? Was he able to eat food?
>> Uh with some assistance on discharge he was not able to feed on his own.
>> Ah so that means even the upper limb improvement is only partial. Am I right?
>> Yes sir.
>> The quadric persist is persisting. Am I right?
>> Yes sir.
>> Only the respiratory problem cleared. Am I right?
>> Yes sir.
>> Okay. Okay. Then he was able to lift upper limb of the couch. Okay. Fine.
Subsequent again he developed pain in both the limbs pay medicine has given bedridden bedridden and the upper limb movement I don't know what is the status of the upper limb move moment at this point of time was he able to bring his fingers to the mouth >> was he the shoulders >> uh following uh after the discharge he was able to move the upper limb like he was able to take >> marginal improvement in upper limb no improvement in the lower limbs is that right >> yes sir Okay. Next, next. Next, next. Okay. Past history. Now, what is a significant? You have mentioned so many things. What's significant past history was there from this slide.
uh there was uh history of fever with uh there was fever with cough four weeks prior to the onset of this illness and uh uh five five days prior to the onset there was a history of sore throat and cough >> okay one minute you have mentioned three significant uh uh events in the past history >> yes >> let's take up one by one the first one you had mentioned fall do you think that fall is significant or not significant.
Uh it is only trivial sir. No significant.
>> Yeah. Very very unlikely. Very very unlikely. He he didn't lose consciousness. He never got him hurt. I don't think that is relevant at all.
Okay. You're not going to think of a spinal cord injury after a trivial fall and then child developing missing. And yet there's absolutely no sensory involvement so far as you as per the there had been no sensory involvement.
Am I right? You did you mention that that he was able to perceive >> perceive compensation in the limbs.
Okay. Am I right?
>> Yes sir.
>> It was only motor weakness. Am I right?
>> Motor weakness.
>> Okay. Now what about the history of sore throat 5 days prior to the onset of weakness? Do you think it is significant or not significant?
>> Um uh in case of GBS and all there can be fever with the respiratory infection two one to two weeks prior to the onset of the symptoms. Ideally it will be >> it's 5 days prior to answer >> yeah this may not be significant sir >> may not be significant okay now l sent me some names of residents who can also be questioned l please lead me to the other the residents now I'm going to ask open question other than a viral infection okay two things do you think this is a viral infection which has been responsible for gain Bar syndrome occurring yes or no this history anybody can take up the answer question.
Um >> oh >> yes please >> uh it can be so there was a fever with the cough four weeks prior to the syndrome onset so >> no no I'm not asking about the fever with cough here I'm asking about the sore throat 5 days prior significant not significant in what way it is significant okay let me give the correct answer however rare It may be that fever, sore throat 5 days before could also have been dipia though you had mentioned that there's running nose and cough where nasal dtheria is very very rare. Okay. sore throat can be dtheria and this can be a postdtheritic neuropathy or post diptheric gillian syndrome.
>> Okay, >> that's the answer. The reason why I'm saying is that if it is gillian the anticident viral infection or the anticedent which other infection is notorious in gar which are the infections which are which are the triggers for gillian bar.
Okay.
Soal causing Asian paralysis China China made. Okay. one, two, >> uh, Epstein bar virus, cytogallo virus, >> more commonly influenza, >> influenza and even influenza vaccin, hepatitis A vaccin, >> many vaccines including rabies vaccin, >> all can cause syndrome, right? But usually the duration of the gap between the illness and galar is around 2 to 3 weeks not immediately immediately I would have thought kept in mind the possibility of a dtheritic poly neuropathy or postitic gulen bar syndrome that's what I wanted from you again cat scratch 7 months back is totally insignificant again vaccine 7 months back crab of action is again insignificant is a similar weakness etc. Okay. Go ahead. Next slide.
>> Okay. Okay. Rest of the history I think there was nothing except that he was completely normal. Now Dr. Suda or one of your colleagues can sum up the history and give a probable diagnosis before we move to the discussion on physical findings. Dr. Nandakumar, Dr. Mundas, if any of you want to add anything, please add in the discussion.
Anybody? Professor Parvati? Yes, madam.
You can also come up with your comments before we discuss the summary of the case.
Okay, please go ahead Dr. Suda.
>> Okay, sir. Summarizing the history, uh, a 9-year-old boy imized for age developmentally normal, presented with acute onset pain and weakness of both lower limbs with rapid progression to trunk and both upper limbs with respiratory muscle weakness. He was treated with IV medication and mechanical ventilation for 12 days. as weakness was in uh he was discharged on followup detected persisting weakness of lower limbs with the u neuralgic pain.
Okay. Now it is often said that in the central nervous system you identify the cause you identify the nature and you identify the site.
And it is always said that the cause and nature are identified not with physical examination but with history. Only the site is identified by your physical examination.
Now you have a boy who has got a quadriperis. Yes or no?
>> Yes sir.
>> Yeah. Is it a quadriperosis or a flaccid quadripis?
>> Flid quadriparasis.
>> Okay. Is it a is it? So if it is a flaccid quadriperis with some minimal improvement in the upper limbs with persistent weakness of the lower limbs and also the upper limbs with requirement of respiratory support for some period with recovery from that with persisting flaccid weakness.
Right?
>> Yes. Where is a lesion? What is a lesion?
>> It is an element type of lesion. Uh >> okay. It's a Okay. Why not just be a spinal shock in an upper motor neuron lesion transsection of the cord?
>> Uh there was no sensory level in this case.
>> Absolutely. There is nothing sensory happening. So I don't think you're going to consider that and if it is an upper motor neuron now he's now bedened for how long now?
>> Two months sir >> 2 months by now spasticity would have developed. Other question is is he having paraplegia in extension or paraplegia and flexion?
Is he having paraplegia in flexion or paraplegia in extension?
You get my question Dr. Sa?
>> No sir.
>> Is he having paraplegia in extension or paraplegia in flexion?
>> Um flexion.
>> Why am I asking this question? Flexion.
Is he keeping the lower limb flexed or extended?
>> Um >> did you ask the mother the question?
>> No.
>> Did you ask the mother the question?
>> No.
>> Pardon? No sir, he was >> okay. On examination you found him to have paraplegia and flexion or paraplegian extension. Uh >> the knees slightly flexed.
>> Mildly flex. See basically you must remember there are some fundamental differences between paraplegia in extension and paraplegia and flexion. In fact, this those those days the the medicine department professors used to ask this question old question but still relevant. They said in general in general any paraplegia inflection has got a poorer prognosis than paraplegia in extension.
Okay. If this boy has got a paraplegia in flexion it's a poor prognostic factor.
Second, if it is a paraplegia in flexion, there may be flexar, spasms and mass reflex.
And in general, paraplegia in flexion, children or adults won't be able to stand.
In general, it is more severe and it is a flexor tone which is more in paraplegia in flexion. These are some of the points. On the other hand, if it is paraplegia in extension, the prognosis by and large is better.
Okay, these patient might even be able to stand and more hypertonia will be there in extens rather than in the flexar. These are clinical method books. Okay.
>> Okay. Right now at this point of point of time do you think he's got an upper you said he's got a lower motor neuron leion do you think he has got a sensor involvement or autonomic involvement?
No. Am I right?
>> Yes sir.
>> He doesn't have bowel and bladder involvement. Okay.
>> What is the level at which the lesion is there?
Level level of leion. uh uh on uh readmission. Um >> no no from the history from the history where do you think is the problem which part of the see okay now let me ask you if he has got a quadriperosis which is flaccid a flaccid quadriperis can occur because of a lesion in the in any of the areas which I'm going to ask Okay.
>> Okay.
>> First is from below upwards. Below upwards.
Okay.
>> Is there a lesion in the muscle which is causing flaccid quadripesis in this boy?
>> No sir.
>> Why?
>> Uh in myopathy it will be more of proximal weakness than this.
>> Proximal proximal and this sort of pain neuritetic pain is very very unusual.
unusual, right?
>> Yes, sir.
>> Right. So, it's very very unlikely unlikely to be myopathy and it looks like an ascending paralysis. It doesn't occur in myopathy. Number one. Second, do you think he has got a lesion in the my neural junction?
>> No sir.
>> No. Why?
>> Periodicity.
>> No.
>> There's no variation, right?
>> Yes sir. And there's no involvement of the facial musculature, ocular musculature, respiratory distress is completely gone after that. Okay.
>> Yes.
>> Very very unlikely. Very unlikely. Then could it be in the peripheral nerve?
>> Uh it can be in the peripheral nerve.
Sir, >> what what makes you think that this could be a peripheral nerve less? Uh there was an um progressive weakness which is an ascending type and symmetrical uh >> okay >> then um there was associated pain like neurologic pain.
>> Okay. Okay. Suda you can switch your video on for better communication. Yeah.
>> Okay. Yeah. Yeah. Okay. Right.
I mean >> it could be in the peripheral nerve because initially he had some pain >> and later he developed ascending paralysis which is very characteristically that of a neuropathy neuropathy >> isn't it >> then could it be in the anton cell >> uh and horn cells no sir >> why why no Why no?
Usually usually you know lesions in the anterior horn cell don't cause this sort of ascending paralysis. ascending paralysis.
>> Okay.
>> Two in the history you could have mentioned that there is no involuntary movement like faciculation that would localize the lesion at the entre cell and you won't get this sort of sensory symptoms. You won't get this sort of sensory symptoms. Again in antrehorn cell of course the the most notorious being your polomiitis.
You won't get this sort of completely symmetrical paralysis. There is absolutely no asymmetry at all. No asymmetry. Okay.
>> Yes.
>> Right. Now last is there a central? Is there an upper motor neural in this child?
>> No sir.
>> And the whole thing is spinal shock.
That's why the child is hypotonic.
>> Um no sir.
>> Why no?
>> Why no?
uh if it's a spinal cord and all there will be there can be bowel bladder involvement.
>> Yeah obviously obviously the other thing is you know a quadripis occurring due to a upper motor neuron lesion.
It will occur only in a something like a transsection where there is initial flacid weakness followed by weakness. Okay, that is not the story here. That is not the story here. Okay, rarely you know venus sinus thrombosis parasittal menoma they can all cause diplesia or flastic paralysis and then proceed upward. they they they are very very rare and no central disturbance appears to be happening. Let us go on to the physical examination.
>> Okay.
>> On general examination the child was conscious oriented in time, place and person. Uh lower limbs lying on the bed uh externally rotated uh no palactus clubbing ed or lymphopathy. Uh vitals heart rate was 96 per minute with the regular ether. Normal volume and character, respiratory rate 22 per minute, regular abdominal thoracic uh no paradoxical breathing. Uh BP was 110 over 70 mm mercury in the right upper limb lying down position. There was no postural variation BP temperature and saturation normal.
>> Please go back to the previous slide.
Please go back to the previous slide.
Previous slide.
Yeah.
Okay. See, basically in pediatrics is always better to describe what you see initially.
So if I were you, I would have mentioned something about whether he is ill looking or well-looking. Is he welllooking or ill-looking?
>> He was welllooking sir.
>> Well-looking. Okay. He is malnourished, obese or appropriately nourished. Uh he was obese initially on prior admission.
>> Now now on examination is he looking obese, malnourished or he is fairly nourished?
>> Fairly nourished sir.
>> Ah you could okay is he cooperative for your examination?
>> Yes.
>> Okay. Another thing is right on examination you mentioned that lower limb lying on bed externally rotated. Is he having good movements of the limbs? Limbs.
>> Lower limb. No sir. Lose no.
>> Yeah, you should mention that he tends to have very little movements of the lower limb. So in the first statement itself, you should appre you should make it very clear what are the arresting or alerting signs. That is that is the essence of pediatrics. Please go to the next slide.
>> Yeah.
Yeah.
Yeah, >> it was normal 96 per minute regular uh respiration rate 22 regular. There was no paradoxical breathing. BP was normal.
No postal variation.
>> Go ahead. Next >> on head to foot examination.
>> Head size shape normal.
>> No facial dysmorphism. Throat was normal. Uh trunk normal. spine no tenderness or any deformity. Uh there was wasting of both upper limb and lower limb mainly the arm and thigh muscles or distal wasting.
>> Uh wasting was more visible in the proximal part >> proximal. What about the small muscles of the hand or feet?
>> Uh small muscles of the hand were normal.
>> Okay. Okay. Go ahead.
uh there was no diaper rash bed so scallosities or contraure of the limbs.
Uh there was single cul and hair nail external genitalia were normal.
>> What is the significance of ku at macule in a child who's got paraplegia or quadriplegia?
Anybody can put in the chat box any student kio macules in a child who has got very important ma the neuroma neuroma neurop fibromyitosis can present with extra medillary cord compression.
Okay.
>> Okay.
>> Okay. Right. Somebody had put neurop fibrotos. Okay. Go ahead.
Yeah, next slide. Yeah, nutritionally is all right. Let us not waste time on nutrition in this case. DMA is okay.
Head size is okay. Right. Go ahead.
>> Examination nervous system higher mental function use conscious oriented to time place and person cooperative attention memory speech intelligence was normal.
No delusion or hallucination.
>> Uh examination of the cranial nerves. uh first cranial nerve able to persist normally.
>> No no don't worry about it. You what are the cranial loss which are abnormal?
>> Only facial was abnormal.
>> Facial. What is the abnormality in the facial?
>> Uh the wringling of forehead was absent bilaterally. Uh he was able to open uh closed eyes without much difficulty. It was able to open and when asked to say e the angle of mouth deviation was less on both sides and the blowing of cheeks was weak.
Okay. If I were you, I would have asked the mother something even in the history to say that he has got bilateral low lower motor neuron facial policy. What questions?
um how the child sleeps uh when >> ah very very important somebody has already put in the chat box very important in fact but all gulan bar in fact I I I have known PG is missing biological facial weakness biological facial weakness is not easy to make out not easy to make out because the m there won't be any asymmetry moments the best way to diagnose is to ask the mother how you sleeping Okay, the eyelashes won't be tucked in right that's a pro to the bilateral weakness and the commonest cause of bilateral facial weakness is giary syndrome so that's a very important physical sign and the symptom you should enquire in all cases of bilateral uh in ginar syndrome okay >> yes >> right and one more thing when uh They you know even unilaterally when there is a bell's paly or a facial pulsy the child even during recovery it may be difficult to appreciate minor weakness.
The best way to appreciate weakness is to identify the difference in the eyelashes getting tucked inside. Ask the child to close the eyes like this and if the eyelashes are easily visible that means there is lower motor neuron facial weakness complete hiding of the eyelashes should takes place if the facial pal facial nerve is functioning properly the upper part of the face. So minor differences can be missed. History will give you the diagnosis. Good. Go ahead.
Please proceed.
>> Uh other cranials were normal.
>> D it's not playing in this presentation.
>> Video of what? Um movements >> normal >> okula movements are normal sir. Uh >> go ahead. Doesn't matter if the video is not playing.
>> Uh motor system bilateral ban are normal.
>> Uh except facial all other cranials were normal.
>> Okay. Okay. U one more thing. One more thing. One way please go back to the previous slide.
The boy looks cushing to me.
You could have asked the mother whether he was like this two months back.
>> Uh he was obese. He was more chubby on admissions. I was obese.
>> Obviously. See that's what that's what I said the power of general examination.
You could have mentioned that he's looking a little puffy. Again you could have verified to the mother. See all things history will help ma.
>> Yes sir. And you can always say he looks cushing because I asked the mother he has put on weight after the hospitalization and IV medication. Fine.
He looks to me a little cushing.
>> Okay.
>> Okay. Go ahead.
>> Uh those uh wasting of the arm, forearm and all >> bilaterally but equal. Uh then downing is more proximally or distally up. Um proximally it was more visible sir.
>> Go ahead.
>> Uh down on inspection he was lying with the upper limb extended at the elbow, arms close to the trunk and lower limb was abducted and externally rotated at the hip. Uh bilateral knee mildly flexed and lateral b of the foot touches the bed. M >> on palpation the muscles of both upper limb and lower limb were flabby and passive movements there was hypotonia of both upper and lower limb >> proximal or distal distal is more proximal is more >> uh lower limb both were uh equal sir >> upper limb >> upper limb was more proximal >> okay you mean say his hand finger movements are good >> finger movements are good >> good >> he was he was able to hold glass without filling >> is he able to handle a spoon.
>> Uh yes sir, it was able to handle.
>> Go ahead.
>> Uh power uh shoulder uh shoulder and elbow for both side it was flexion extension abduct adduction was grade four in upper limb. Uh then wrist also grade four.
>> What about the power of the neck muscles?
>> You didn't mention upper limb boyis. Don't you think that is important?
>> It's in the next slides. Neck flex and neck flexes >> should come first. It should come first.
>> Okay.
>> See, come from above.
Okay. Go ahead. Sorry.
>> Finger the lumbricals in open grade three in power.
Uh then uh the lower limb uh uh hip uh hip flexion extension all the movements are on grade three power >> and knee also grade three uh angle dorsif flexion was uh grade two and planter flexion with the toes only a flicker flicker of movements only in the toes grade one uh neck >> flex symmetrical flaccid weakness of all the forms more distal than proximal more and more in the lower limb than in the upper limb. Am I right?
>> Yes sir.
>> And neck muscles.
>> Neck muscles are grade four power extensors and flexes. Uh abdominal abdominal muscles amus is the midline normal power. Uh respirator muscle no weakness of diaphragm or intercostal muscle. No paradoxical breathing on splending the diaphragm. There was no distress and all.
Chromastic was present or absor come to the reflexive. Okay, go ahead.
Um then reflexes superficial reflex uh conential was present. Coral node tested. Uh abdominal was absent in all four quadrants. Uh plantar was mute bilaterally. Cremastic was absent and uh deep tendon reflex uh all biceps, triceps, super and angle check was absent bilaterally. What about Jo?
>> Uh Jo was absent sir.
>> Okay.
Go ahead.
Uh sensory system uh it was touch paint and ratio was normal. Vibration position sense was normal. Uh state hypnosis to upon discrimination graphicia normal. Uh there was aloa in bilateral leg and uh food.
>> What is aloa?
>> Um uh abnormal uh the other sensation will be perceived as pain. Um >> okay. Okay.
Go ahead.
>> Uh cerebella signs >> plant response. You have the video. No.
>> Yeah, I have the video sir but >> doesn't matter. So what is the plant response you got? It was mute pilot absent response both >> absent. Okay. Okay. Fine. Fine.
>> Go ahead.
>> After the presentation you can show all the videos separately.
>> Okay sir.
>> Okay.
>> Uh cerebella signs upper link finger no test was normal. No intention trauma distenia absent. Lower limb could not be assessed. No involuntary movements. No peripheral nerve thickening. No neck stiffness. Kne and Brinsky was negative.
>> SLR test there was pain in hamstring muscles on straight leg raising skull and spine was normal.
>> Autonomic nervous system normal. No postal hypertension, excessive sweating, flushing or urinary attention.
Respiratory system was central.
Desperate rate was 24. Breath sounds equally heard on all areas. No grapet or wrong. No paradoxical breathing. What other wait wait wait wait wait.
Respiratory system something more important than whatever you had mentioned should have been mentioned.
>> Anybody can put in the chat box.
>> It is a bedside test in all syn.
>> Ah that's very very important. should not forget breath count.
>> Yes.
>> Okay. It's a very noninvasive simple method. You don't even need a AG to pick up early respiratory distress failure and paralysis.
But you should put a chart.
Okay. Okay.
>> Very very important and it's must one.
Second, in a case like this, you should also mention whether you try to elicit paradoxical breathing.
>> Yes.
>> You must remember there are two types of paradoxical breathing or paradoxical respiration which should not be missed on clinical examination.
the seessaw seesaw movements for example you take you know not relevant in this child you take word hoffman disease or spinal muscular atropy in spinal muscular atropy for reasons poorly understood diaphragm does not get involved until the last and the seessaw breathing will be there. The abdomen will be moving nicely but the intercostals won't be moving. You can actually splint the chest and the baby will still be having paradoxical breathing of movement of the abdomen.
On the other hand, if there is a lesion which is affecting the intercostal muscles and not the diaphragm, if you press on the diaphragm, there will be hardly any movement of the chest because intercostals are weak.
Intercostals are weak. There won't be any movement. So you should be able to identify paradoxical breathing. And by splinting the chest and abdomen once differently, you should be able to appreciate whether the respiratory paralysis is due to intercostal weakness or diaphragmatic weakness. And diaphragmatic weakness is very late in spinal muscular is almost faciciculation.
And the paradoxical breathing with diaphragm being intact are nearly confirmatory signs for diagnosis of spinal muscular atrophy. That too the infant is alert.
No central involvement. It is happen clinically and nothing else.
Okay. Please go ahead.
Uh cardiovascular system affects in the left fifth interostal fourth interostal space clavicular line normal heart sounds gastrointestinal system those carries to abdomen soft non tender no the may bladder notable external genital was normal >> okay one another physical finding well very rare I have seen only one or two cases is you should always palpate the peripheral nerves, peripheral nerves, poplial nerve, alna nerve. Try to find out if there is any thickening which may give evidence that the whole disease is falling neuropathy, peripheral neuropathy. Of course, not in this child, but there doesn't seem to be any sensory involvement. But I'm just telling you for completion for of examination also mentioned that you tried to palpate the peripheral nerves.
Okay. Go ahead.
Summarizing the strain examination.
Nine-year-old boy immunized for age with a normal development presented with history of symmetric lower limb pain and weakness with a rapid progressal ascending paralysis of 3 days duration with hypotonia and a reflexia of all four limbs 2 months back. He was treated with IV medication and mechanical ventilation were 12 days. After discharge the weakness of both upper limb improved but lower limb weakness was persisting. On examination there was bilateral facial weakness. Upper limb power was 4x5 and lower limb power 3x5 with hypotonia and a reflexia of all four limbs. Uh distal more than proximal weakness. Lower limb weakness more than upper limb. Uh sensation was normal. No barbar weakness and no autonomic involvement.
>> Okay. So what is your complete diagnosis?
>> Um complete diagnosis will be it is a case of acute flax paralysis. uh uh mostly element type of uh in this context uh I will sus >> now how long how long is the paralysis >> huh it's there for months you still want to call it acute flaccid paralysis >> no sir >> I think you should straight away sayronic chronic quadripis >> chronic it's more than two months >> more than >> okay of course exam wise if you say acute flaccid paralysis always better.
Okay. Though I wouldn't call this acute anymore. 2 months now over. It's a chronic quadriperis which is flaccid.
>> Flaxid.
>> Okay. Right. Now yeah please give a complete diagnosis before we start discussing.
>> Um it is a chronic quadripis mostly gillenbaris syndrome.
>> Okay. Okay. Why do you say that this is Gillian Bar syndrome?
Um and the presentation is like symmetric uh ascending type of weakness uh with uh with some pain and pain in the lower limbs initially and u it was a a progressive type of weakness with the uh later involvement of the uh facial respiratory muscle involvement and uh um after that uh child uh like The improvement is from uh improvement in the opposite direction. Upper limb was improved first with the mild weakness of lower limbs persisting.
>> Okay. Okay. Now if you know this is straight for I mean clinically I don't think we have any other diagnosis other than Glen Baris syndrome in this child for the following reasons.
One, it is a symmetrical flaccid paralysis.
Second, there is no sensory involment objectively on clinical examination.
Third, there is bilateral facial nerve weakness.
Okay. So, clinically, yes, agreed.
There's no other differential diagnosis.
reflexes are absent. So it is Gillian Barry syndrome. Now I'm going to ask you an exam question.
What are the features?
What are the clinical features or invest?
Can anybody put in the chat box when do you what are the clinical features which caused a doubt in the diagnosis of Glen Bar syndrome?
>> Yes sir.
>> Uh if it was an asymmetrical type of fitness.
>> Excellent. one is and in fact if I remember reading the uh uh you know the Brighton criteria market persistent asymmetry beautiful adjectives I still remember market and persistent asymmetry that's the most important red flag we should tell you that is not like let me go in one two >> um uh if there was any u fever at the onset >> excellent Fever at onset.
If you have fever on day one and the child comes with paralysis, it's not Gary.
Fantastic. It's a post post infectious immune phenomena. Two, three.
>> If there was a definite sensory level, >> absolutely right. There is a sensory level. Three. Four.
>> Four.
Investigations.
>> Investigation.
which which will tell you that this is not Glenber syndrome. uh if the CSS CSF is showing uh total count more than 10 mean >> not 10 not 10 up to 50 >> 50 >> 50 up to 50 >> if the CSF is showing more than 50 cells per cubic mm it's not gary >> straight away >> right >> yes >> and one more clinical clue if you have very early in the course significant bowel or bladder dysfunction it's not gir Whatever bowel or bladder dysfunction that may occur rarely in glen body is transient and it doesn't occur very early on day one or day two or day three that's another thing so just to sensitize PG's listening please think of diagnosis other than gillian body when there is market and persistent asymmetry when there is a sensory level when there is fever at onset.
Okay.
Rarely when there is hyper reflexia you don't think of hyper reflexia is against genar and when the CSF cell count is more than 50 you should think beyond gillian syndrome though it is said to be symmetrical mild asymmetry can occur transient sensory disturbance occur for every rule there is an exception right yes >> these are the important points now other than gillian bar syndrome What other diagnosis did you consider in this child?
>> Uh nonpolio endrovirus infection.
>> Nonpolio entrovirus infection.
Okay.
What are the points for for and against?
>> Um it was simplitis because I discouraged you. No sir, >> I'm mentioning see but having said that from the exam point of view if you asked what are the other causes you should go by the commonest ones the commonest four causes of acute placid paralysis is gillian body worldwide it is the most common today right second is transverse malitis >> yes >> third is polomiitis or nonpolio entraviral infection which can cause last is the promatic pneum Okay.
>> Yes.
>> Now, in this child, you're not going to consider traumatic neuritis, >> right?
>> No.
>> And you're not going to think of paralytic polioitis. Though in terms of public health significance, you have to investigate, right?
In addition to nonpolio virus, what other virus infection is emerging as an important cause for such acute flaccid paralysis in the world? Can anybody put the question answer in the chat box?
>> My plasma adino virus.
>> I said viral infection. Anybody?
Anybody has put in the chat box? Let me see.
Okay, the answer is Westnile virus infection.
Westnile virus infection mind you is a mimicker of polomiitis.
It is emerging as a cause for acute plastic paralysis in Africa as well as in America. India I don't think they have there are I think one or two case reports I remember seeing in addition to coxi virus you have to consider this but the point against this again absence of fever hyperacute ascending paralysis right makes that very very unlikely. Do you think this is transisitis?
>> No sir.
>> Okay. Why? Absolutely no sensory bladder involvement at all.
>> Other than this, other than this, what are the other conditions which can present like gillian bar syndrome? Did you think of any of them?
Suppose you had seen this boy on day two, day three of acute flaccid paralysis.
What other conditions would be considered in the differential diagnosis? Suppose suppose this boy has got some CNS disturbance and the mother says he's passing a very orange color urine and he's also having severe abdominal pain >> perfaria >> parf how rare it is perferia okay perfaria abdominal pain this sort of presentation simple urine test will confirm the diagnosis >> you must look at the color any acid flaccid paralysis. Please look at the color of the urine and rarely you said bottism and you know amoglyide use massive you know intraabdominal installation of cannamyin gentamy can cause or aminoglyide can cause a mthenia like paralysis right and uh sometimes a tumor can fool you. Tumor can fool you but it cannot fool you for two months. Here no other symptoms of C compression. No systemic signs are there. Right? And of course in the initial stages first two days if you had come to you definitely you would do electrolytes to load hypoc calmic or hyperc calmic >> periodic paralysis periodic paralysis >> and myastthenia won't present like this there is absolutely no involment of the ocular muscles there doesn't seem to be any periodicity at all so all that is very very unlikely okay now basically you must remember whenever you have a child who has an acute paraplegia few other conditions have to be thought of. Can you think of any other infectious disease emergency when there is a paraplegia or quadriplegia? I said infectious disease emergency.
Can anybody put in the chat box any acute infectious disease emergency which can cause acute weakness like this excellent epiduralis Dr. Rapura has put it high fever sorry tenderous or the spine luccoytoosis epiduralapsis only a surgeon can cure it life saving life saving okay not infection okay not inflammatory not so but acute paraplegia back pain is is there back pain is there neck pain or spinal pain you can't diagnose clinically >> disc prolapse >> pardon disk prolapse will have severe pain mark anybody malfformation of the spinal arteries leading to thrombosis hemorrhage.
I have seen one caseia pain acute paraplegia of course both motor and sensory but primarily motor healia.
Okay. And rarely rarely you know anterior cerebral artery stroke can give rise to acute parapalysis or unpair the anterior cerebral artery meniomas.
Okay parasittal meniomas parasittal tumors even cerebral venus thrombus can cause paraplegia. Of course you should not forget hypocalemic and hyperc calmic periodic paralysis and as you had mentioned both your you mentioned snake bite and you mentioned scorpion sting and snake bite they can cause and of course you must you must always think of gileian I mean gileian body syndrome following dtheria dtheria the only thing is in in post dipthertic paralysis the nerves which are often involved are which nerves are involved in postitic paralysis commonly >> extra muscles >> no extra which okay extra you're not wrong what is what is a what is a what is a peculiarity about that okay in postitic paralysis there are two things which are very distinct and peculiar which doesn't which don't occur in any other disease one is paralysis of accommodation convergence.
Okay, pupils will be reacting nicely.
But if you ask the boy to look at a distance and then take the object close to his eyes, he won't be able to accommodate. That is very very peculiar to postitic paralysis. One two in postitic paralysis they often present with nasal regurgitation of fish due to paralysis of glossopherrenial and veagal nerves that's very very peculiar these two peculiar paralysis don't occur in any other condition other than post dipritic paralysis in fact I've seen at least two or three cases nowadays we don't see them often we used to see them quite a lot four decades back three decades back not No.
Okay. Right. Then how do you investigate this child?
What did you do for this child? Can you you have the list of investigations and what do you do? Please project the investigations that you did.
>> Of course, the first investigation you should do >> is your duty to the public health. you should immediately inform the >> publicistic immunization officer >> and of course collecting the stool sample etc. I'm not going to waste time on on the theory part of it. You please tell us what you did and project the investigations.
Please go ahead.
>> Okay. Come uh complete complete blood counts CRP then electrolytes CPK RFT LFT. Uh then uh after one week we have done the CSF analysis which cells less than five with the protein 188. There was alpinocytological dissociation in CSF study. Typical. It is very typical.
Cells are not high. Protein is very high. It it it corroborates with your clinical diagnosis of glyian bar syndrome. Agreed.
>> Uh then we uh we done MRA spine and brain screening which was known.
>> One minute one minute one minute. What is the role of MR in a child with Gen syndrome?
Does it have a role or no role?
So I'm asking you an exam question.
What is the role when do you do MRI in a child with Genar syndrome?
>> Can anybody can anybody excellent answer Dr. Rapura has given only if you have a diagnosis in doubt and you're thinking of a say a spinal cord compression healia other diagnos when your diagnosis is doubtful I also gave you a list of features which make you doubt about the diagnosis of Glen Bar syndrome if they are there you should do MRA otherwise MRA particularly has no role in confirmation of diagnosis of gillian bar syndrome. You can only rule out a space occupying lesion uh uh uh hematomeia epidural abapsis.
Okay.
>> Yes sir.
>> And not confirm the diagnosis of gillian bar syndrome. That should be your answer. It's not mandatory. Okay. Please go ahead.
uh then nerve conduction was study was done. Uh we showed a motor nerve conduction study showed absent response in bilateral tibial perona and uh a f study showed absent response in bilateral median and alnar tibial and perona sensory response was relatively maintained. Okay, I unfortunat for fortunately or unfortunately I don't know what the nerve conduction studies show but all I know is that nerve conduction will confirm the physiological changes that occur in gill bar syndrome and they are also helpful suppose the nerve conduction is completely normal it is against a diagnosis of gillian bar syndrome that's all I know and there's no emergency to do nerve conduction studies you the obvious features may may be delayed also in the electrophysiology. Please go ahead.
>> Then AFP reporting was done. Two store two samples were sent. Uh throat was taken for viral study which was negative. CS viral study was also negative. Chest X-ray was normal.
Uh then uh this was in the first admission and the next admission we done the nerve conduction study which showed um uh there was reduced amplitude in the bilateral sural nerves. So there was some sensory now involvement.
>> One minute. Please go back. Please go back. Go back to the previous slide.
The history of cat scratch.
Okay.
What other investigations would have been appropriate. You have done everything.
You have done CSA viral studies and all.
In fact, I wouldn't have done viral studies for this case because protein is high, cells are less than cells are only five. What's the point?
Right? Tell me what other investigation I would have investigated for rabies rather than >> viral studies because there is history of cat scratch and rabies can very well cause ascending paralysis.
>> Yes sir.
>> Okay. It can behave like Julian B.
>> Yes.
>> Right.
>> Yes.
>> Only thing by this time should have should the child should have manifested with the you know hydrophobia which has not come. Right. Go ahead.
>> Yes.
Go ahead.
>> Repidal conduction study done show serious symmetric moto predominant neuropathy involving both upper and lower.
>> So did they did they give a reports consist of my knowledge is very primitive. I mean they they divide that into you know ammon and adip etc. I don't don't understand much to different types whether the the nerve conduction they study gave clues to specific type of gillian bar. No >> the no sir they gave impression like this only but uh the first one >> I okay let us not discuss since I don't know much about it honestly please go ahead and somebody more intelligent a neurologist can only give an input on this my apologies. Next >> uh this is where the investigation done sir. Then um he was treated with the IVG initially. Then for pain we gave uh gaba pentin and neurobion for pain relief.
>> I know the investigations.
>> Okay. Only thing is you should also remember rarely you can have a child who has got subacute combined degeneration of the cord secondary to B12 deficiency with anemia and paralysis like this okay that's a rare even thamin deficiency can present like this rarely child doesn't seem to have any other features suggesting that okay go ahead H >> yeah.
>> How did you treat him with >> he did he receive IVIG or steroids or both? IV sir we gave 400 mg per kg per day for 5 days when given supportive treatment uh initially given mechanical ventilation gradually we ended off uh as watched for any features of bulbapuly was not there then he was started on slowly feeds uh then started on physiootherapy uh nutrition was advised >> then for pain >> nowadays Now they do some specific antibbody test which I don't know much they report some cases which will respond better to infleximab or monoconal antibodies better than steroids and refractory cases they do some uh specific tests I I don't know much about it if anybody knows you can you can learn from your neurologist okay that's what they do right Okay. Anything else you want to add?
>> No sir.
>> Yeah. Okay.
>> AntiGM1 ganglo antibodies.
>> Pardon?
>> Antiganglo said antibodies >> they are useless. I don't think they some new tests have come where they predict good response. Some syndromes they are describing where monoconal antibodies like infleximab might be of help. some predictors I don't know you can go and look up or ask your neurologist okay >> okay okay >> very good presentation Dr. Sana if you present like this you will get a distinction from me in the exam >> thank you sir >> okay undoubtedly okay any comments from Dr. Mandas.
>> So then what was your comment about the muscle bulk?
>> Uh >> muscle biopsy muscle biopsy. Why for this?
>> No, not biopsy sir. Muscle bulk. What was your comment?
>> Uh there was wasting compared to the previous admission sir. Previous admission he was looking obese with the good muscle bulk and all. And the second admission there was some wasting both upper and lower.
>> Okay. Mandas you would have seen the case. Can I add any any valuable comments?
>> Uh the important thing is that the even though child had shown some initial improvement now the weakness is persisting no much improvement. So thinking that there is aopathy.
M I think uh you can consider the other differential diagnosis and even consider monoconal antibodies depending on the type and further imunological studies.
Okay. Uh my knowledge is quite superficial with regard to that. Right.
You presented very well as sir was >> did a very good job. Congratulations was pointing out there was a confusion in your presentation about the upper limb weakness and wasting.
So basically it was a weakness a dist weakness and it is all expected also.
But uh when you mentioned about the wasting you said the wasting was more in the proximal part.
So always be careful when you're presenting should not be contradicting your power part wasting part and the urls also should be correlating should not be contradicting that's one.
Did you do the microplasma antibody because the patient presented?
>> Yes sir. Mopo plasma IG was it was negative. offer that is >> yeah but my I'm afraid I think doing now any studies for micro plasma that after administration of IVIG uh thing and there was never any respiratory manifestation and the the the you know it's a very controversial area unless the child is acutely ill with respiratory manifestations fever and then along with that neurological manifestations are immediately following the severe febriel illness neurological manifestation. The cause and effect relationship of mitoplasma causing all this uh is something which is very very controversial. And if you want to prove that it is my plasma, unless you get a PCR positivity in the you know in the lower respiratory specimens or a PCR positivity in the CSF or a four-fold rise in IGG antibodies, I don't think my plasma should be considered as one of the differential diagnosis in a child who has got chronic illness like this, chronic illness like this.
So in 2024 we had an epidemic proportion of microplasm. We had all these things at that time. We had many cases of atypical presentations, neurological problems including strokes. We had we had these hematological complications, renal complications. Huge numbers were there. But luckily from 2005 onwards that much of numbers and complications are not seen. Another another one we had few cases of this enroiruses also epidemic proportions handful of disease and neurological complications.
We had many cases of proved uh sika virus but luckily non neurological complications so far. So that is a one entity which we need to worry in the future. We had a sir was pointing out about the west nai. In fact in Kerala recently we have started added two more district. One is kalicate another one is malapuram for jabian caparatus but the data shows that the recent incidences of ji is less and more number of westnile is reported especially from the northern districts and last year we had four case of westnile but no complications or death. So the snail is not that rare but many of the cases presented with the the eniphatic form of course as you said can be an associated uh peripheral uh angle capsence and the weakness also predominantly but the acuteic syndrome like presentation and just like jabi the extra pyramidal plus pyramidal and the element science also that's the combination which we used to get in this thing But luckily that also didn't produce more of a mortality.
The S was pointing about the last part of the nerve conduction studies that is one thing the F waves and one thing is the sensory or motor ammon type of things in this case sensor is not there. When there is a motor again, what is the is it a conduction problem or the the amplitude problem in a case of the the demiation type the response will be much better with your monom modulators and the the the conduction uh the latency part will be more involved not the the the motor uh volume or amplitude. So in a case like this where the the response is poor the the weakness is still persisting at 2 months very likely that the external involvement is there predominantly the the amplitude of the compound motor action action potential action potential cap will be low it is not the conduction part it can be a combination also so in this case as pointed out when the response is not there newer and newer modalities gamma are not responding, repetition, not responding, we need to go for a trial with monocon antibodies.
Also, uh in initial part you discussed very well lot of prognostic points which are pointed out how fast the weakness progression uh uh the the progression to the lower corer part was discussed and uh earlier part very very well discussed. s covered all the all the possibilities also.
Thank you. Thank you.
>> Thank you very much sir. It's so nice to have you have you and your comment. So nice.
That's why I said you need more intelligent people to decifer nerve conduction study and other complex issues which you you nicely elaborated.
Thank you very much sir. on the other interesting thing uh you know all these uh syndrome in fact I still remember my old professor of neurology he used to tell us what in 1983 I still remember his uh classes uh he used to say that uh the entire spectrum of diseases like you know adm M to guillian bar can be grouped under antibbody syndromes against the myelin sheath or the protein and they can all be called or put in one big group and that group can be called enkafalo meaningo myelo radicular neuritis I'm repeating it encap meo myelo radicular neuritis and most of these diseases are because of molecular mimicry the body produces auto antibodies against the myelin sheath protein and you know it's like Iranian missiles the the missiles go and hit several places in the nervous system. If it hits the brain, it becomes enkaphilitis. If it hits bits the hits the manas more, it become meningoilitis.
If it hits the ant if the hits the peripheral, it becomes gillian.
So all these are antibbody syndromes and I'm sure maybe 5 10 years from now we will not be giving Ivag or steroids we'll have specific monoconal antibodies to destroy those antibiotics or neutralize those antibodies that is one. Second, in the west slowly and steadily plasma ferosis is taking precedence over IVIG and quite a few adult studies have shown plasma ferosis may be superior.
Okay, thank you very much sir.
Yes, Dr. Any other comments from senior faculty?
>> What about the president sir?
>> I think he has left for another meeting.
>> It's okay. It's okay. No problem.
>> Will you please show your video?
You are the mentor and we >> compliments to the mentor Dr. Arushi.
You have prepared the student extremely well. In fact, she knows more about Gillian Barry than what I know. That's one of the reasons I wanted to be blinded. I didn't want to know anything about the cases.
It always is better to learn.
>> So then when you mention about the facial policy, there is no need to mention about the deviation part. Sir was pointing >> it is when you are getting a bilateral problem, you don't expect it.
>> So you sir explain that how to detect the bilateral weakness where you should be looking for the root of eyelashes is to be looked for sir said >> and one history whether the child can drink use this straw that is one point you can ask >> okay sir >> very useful Can you try that video?
>> Type of gimber is there sir. Predominant sensory involvement also is there sir.
sensory type.
It need not be sensory feeling only. Documentation documented sensory loss and nerve condition study shows the sensory nerves action potentials are normal. you can classify that sensory GPS. So in a case like this there can be sensory feeling and what the child described. So it can be that but prolonged subjective feeling is less likely >> sensory is very very rare >> Dr. Sa one comment on your you should improve your technique of eliciting the deep tendon reflex.
>> Okay.
>> Your your your wrist was moving more than the elbow.
>> If it were my professor, he will give me a fat like this on my hand. If I do like this, he'll kick me. Okay. See I always used to say that you know when you are eliciting you know the kneejerk or with the hammer you should only move your hand like this not like this. This is what you're doing that is wrong. I hope you get it. Please see my >> you should move only like this not like this. In fact I used to tell my students go sit in your mess.
Sit on the table like this with your left hand like that. Keep on tapping moving only the wrist. That's the best way to improve two methods. One elation of deep tendon reflexes. Second is percussion of the respiratory system.
There again your elbow should not move only your wrist should move. Comment number one.
Second if you see in the video there is one other finding which you should have described.
See he has got plantar flexion. Yes or no? Bilaterally.
>> Yes.
>> Yes.
>> Yes sir.
>> Yeah. Indicating he has got a he's got a weakness to the >> dorsif flex.
>> Dorsif flexors. See even without touching we can appreciate he has got weakness to the dorsif flexors.
Right. And in fact I could appreciate his gastronomus is wasted lower down particularly in the left side. Yes or no? Yes sir.
>> Yes.
>> So shrewd observations are required in pediatrics. Please go ahead.
Okay, sir. Okay.
Okay. Yeah, please go ahead. It's not moving.
Not moving.
>> Planter is absent, is it? Is >> absent.
>> Okay.
Okay.
Right. Um movements and also um no wrinkling of okay that's screwing the eyes facial Next fold and roll less prominent on both sides and uh there is no wringling of forehead on looking up.
>> Can we end up sir?
>> What about what about the facial rec will monoconal antibodies be helpful at this stage or should mad because only after failure of the conventional drugs only you will go for the monocular antibiotics. How many weeks you wait?
>> Uh initial initial maybe I think 3 months after 3 months only this these sort of studies and trials are there.
It's not of 100% benefit but rather than nothing if there is some benefit can be tried.
>> Thank you can try.
>> Good evening madam.
>> Good evening. Good evening. Good evening. I came just because you are the you are the faculty well presented and well discussed everything good.
>> Okay.
>> Today number of participants were less because of two facts sir it was a happened to be one of the holidays and >> yeah another thing we lost two of our colleagues. I know understandable sir.
>> Maybe the discussion was excellent and people will be following the YouTube later.
Thank you sir.
>> So thank you sir for being with us uh and discussing the case in an exemplary manner and uh thank you Sutena for presenting the case very well >> and Dr. Arushi who mentored the uh student. Thank you all for being with us. Good night.
>> Good night sir.
>> Thank you.
Thank you sir.
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