Guillain-Barré Syndrome (GBS) is an acute inflammatory demyelinating polyneuropathy characterized by progressive ascending flaccid paralysis with preserved sensation, typically preceded by infections like Campylobacter jejuni. The diagnosis is supported by albuminocytological dissociation in CSF (elevated protein with normal cell count) and reduced/absent nerve conduction studies. Key clinical features include distal-to-proximal weakness, areflexia (ankle reflexes lost first), and possible autonomic dysfunction. The 20-30-40 rule (vital capacity <20ml/kg, inspiratory pressure >30mmHg, expiratory pressure >40mmHg) predicts respiratory failure requiring mechanical ventilation. Treatment with IVIG or plasma exchange should be initiated early for optimal recovery.
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SZ SMZ API ICP Master Class Webinar 19th May 2026Added:
Kuman sir, assistant professor of department of neurology. Really thank you sir for joining us and we have with us consultant neurologist Dr. Maria Penser also joined today. Really thank both the neurologist for joining us today and being the faculty for this central nervous system case discussion of chord parases. very essential part of uh or important case scenario for the post-graduates to learn approach towards the corder parasis to present this case we have with us Dr. J Anthony the first person of postgraduate to present this case from Thrive Middle College department of medicine really thank you Dr. J Anthony for joining us today I request the all the faculties Dr. Nadraan sir Maria sir mutukumar and sir take over the further proceedings of the session and start discussing both historical aspect of the patients problem and as well as examination findings and investigations and management as well. Thank you and over to the faculties and postgraduate. Thank you.
>> So thank you very much sir. Thank you and first of all I thank uh Talon and sir Apic chairman and Dr. Saron sir for giving us through our medical college an opportunity to participate in this PG master class. Uh we have been uh just participating from this week and I I welcome my colleague Dr. Dr. Mutan who is assistant professor in neurology and Mario who is a friend of mine neurologist consultant neurologist and now I welcome Dr. J Anthony Pas who is our final year postgraduate who is going to present about this case a case of quadripesis for evaluation for clinical examination and uh mutan sir do you want to say anything sir? No sir also let you start presenting sir before just make a small hint to the postgraduate alone because since the first time you're all presenting and participating I just telling you just Anthony don't get perturbed or disturbed because of the three faculties and you have been cornered by these three faculties this basically this platform is designed for uh committing all the mistakes here so that you don't make any mistakes in the examination and the faculties are going to take you through lot of questions but at the same time the difference between the examination is going to be they'll tell you the answers also. So the only difference between the examination and this presentation is going to be you'll be definitely questioned lot but at the same time you'll be given the answers so that you'll get a best benefit out of making the committing the mistakes and get the clarifications so that you don't make the same mistakes in the the few more months you're going to appear for the exam you will not make the same mistake. Yeah just please proceed sir year after I will not interfere. Thank you.
>> Good evening sir. Thank you sir.
to just start presenting just uh >> good evening sir thank you sir sir presenting an 18year-old female miss ABC residing at thiraru who is a right-handed college student who came to governmentaru medical college hospital with chief complaints of difficulty in using both hands and both legs for the past six days history of presenting illness the patient was apparently well six days back when she woke Woke up in the morning and had noticed that she had difficulty while holding her toothbrush and she felt that she had reduced grip on the toothbrush while put and also while putting her bathroom chapels. She also experienced difficulty in gripping her slippers. Despite these symptoms, she attended the college on day one as you on on day one. While in the college, she noticed difficulty in holding her pen while taking notes and she also had difficulty in mixing foot while eating and she also noticed that she had difficulty in holding the handrails while traveling the bus and she did not have any difficulty but uh but she did not have any difficulty in getting up from sitting position nor she did experience any difficulty in lifting her arms above her head. Coming to day two while attending her college she felt that she had difficult her difficulty in holding pen was progressively worsening and she was able to write only a few pages as compared to her usual note-taking activities. She also noticed that she had worsening of difficulty in uh she has she she also noticed worsening of difficulty in gripping her slippers and at this stage she also but also insinuating her legs in. There was no history of any slippage of slippers without her knowledge and she did not feel any difficulty in appreciating hot and cold sensations while working in her kitchen position and getting up from bed. She also had difficulty in rising from her Indian toilet and required support from the wall to get up. However, at that time she was still able to lift her arms above her head without any difficulty and she was also able to comb her hair although she had difficulty in gripping the comb. She was taken to a nearby hospital with the abovementioned complaint where she was informed that she might be having a vitamin deficiency and was administered one intramuscular injection.
On the fourth day she developed difficulty even in standing up from bed.
However, she did not have any difficulty in rolling from side to side on the bed and because of this increasing difficulty she uh in using the Indian toilet on that on the fourth day she avoided using it and instead started using western toilet in her house. Even while using the western toilet, she experienced difficulty in getting up from the sitting position and she also had difficulty in uh lifting her hands above her head and by this stage she was hardly able to write even a full page of note. Despite her difficulty in using the toilet, there was no history of any involuntary mixuration or involuntary defication.
On this fifth day, her symptoms further worsened and she needed to push her chapels against the wall in order to insinuate her leg into them. She also developed difficulty in walking and was forced to lean against the wall after walking a distance of around 3 to 5 m.
Her difficulty in holding pen worsened further and she was unable to write even half page half page of notes because of the weakness. She was taken to a nearby hospital where she was administered IV fluids and was advised to seek uh care at a higher center. On the sixth day, she developed blurring of vision. The blurring did not worsen on closing uh did not worsen on closing either of her eyes and she denied any difficulty in distinguishing colors and she did not experience any pain on moving her eyeballs and she was able to read and write as well. She was brought to our hospital and at the time of arrival she required support from two people in order to stand and walk. She also gave a history of palpitations. But there was no history of any giddiness.
There was no history of diplopia. There was no history of difficulty in swallowing. There was no history of any preceding vomiting or loose stools.
Although she complained of numbness, she did not have any difficulty in appreciating hot or cold sensation. And she was able to fit clothes over her body as usual. There is no history of any native medicine intake. There is no history of any toxin exposure. No history of any proceeding man vaccination. No history of abdominal pain and no history of any similar complaints in the past.
Sir, can I continue with the past history?
>> Yes. Yes. Yes. Actually based on your history uh you explained the weakness first. How was the weakness? Where it started over a period of days it progressed. No sir. Uh actually this uh weakness started distally in both involving both upper limb and both lower limbs s and after it it ascended and started impro involving the proximal muscles uh proximal limbs within a span of 3 days sir and uh she though she complained of sensory symptoms she was able to appreciate cloth over her body and was able to appreciate halt and hold sensation even in working in the kitchen. On the third day and fourth day she wasn't able to work her in her kitchen but when her mother gave her hot coffee and all she was able to appreciate the heat hotness over the cup sir.
>> So the patient had only sensory symptoms no sensory loss from the history.
>> Yes sir. Yes sir.
>> Okay >> sir. Uh uh can I should I pro can I proceed with the past history sir?
What for the toxin exposure? What are the things you want to rule out for toxin exposure?
>> Sir, I would like >> has got uh almost weakness of all four limbs with the sensory symptoms and uh bubble bladder. You said no incontinence whether she was has she had any difficulty in uh initiating or completing the act of mixion whether she was able to hold the urine whether she had >> no no incontinence sir >> incontinence not whether she's able to initiate >> sir >> and control the act of mixure whether she has got the sensation of complete bladder evacuation also she was not having any bladder bubble symptoms not only in incontinents I'm talking about all other bladder symptoms like autonomic symptoms she had pulpitations whether the palpitations were regular uh uh okay sir yes sir har sir I can hear you sir you're muted sir Hello sir sir.
>> Huh?
>> Yes yes yes yes.
Ah you see now you are able to get me.
>> Yes sir. Yes sir I can hear you sir.
>> Oh yes yes >> sir. Actually this patient didn't have any uh difficulty in initiating maturation or completing. she was able to hold during sir because in the third day and fourth day even though uh she wasn't able to walk she used to like call her mom for her support to go to the restroom sir at that time she was able to hold her urine sir and uh since this patient is having an ascending paralysis along with uh suspected sensory involvement I would like to rule out uh thoughts and exposure in case of um uh any um uh uh uh polycarbon in history of polycarbon like uh benzene uh and other polycarbonate inhalation history sir.
Also I would also like to rule out any uh history of heavy metal exposure sir because heavy metal exposure can also present like arsenic, talium and even gold can present uh kind of arsenic usually mimics closely mimics bulenberry syndrome and patient will be having g symptoms also. You also mentioned about that abdominal pain isn't it?
>> Yes sir. Yes sir. uh arsenic also presents with abdominal symptoms and also some sort of encphylopathy >> abdominal pain enhopathy and quadripes what are the other things we have to rule out >> sir I would also like to rule out in such cases parferia sir pfaria can >> paria parferia will present with abdominal symptoms and quadripises and also psychiatric and neurological symptoms like encphylopathy all these things can occur with acute intermittent perferia also >> yes so arsenic presence classically It mimics colon syndrome.
>> Okay sir.
>> And let it presents with purely motor neuropathy especially wrist drop.
>> Okay sir.
>> Prominence will be there. Mercury will produce only sensory neuropathy mainly.
>> Okay sir.
>> What are the other other toxins late exposure rate?
>> Uh thallium sir >> uh thallium can also that that also produces a painful neuropathy. Here the patient is not having any pain is >> no pain sir. No pain sir.
>> Yes. Yes. No pain. Um other things arenas compounds >> uh sir like monocro oropospherous compounds >> native medicines also can induce antibiotics what are the antibiotics that can induce symptoms like this.
>> So is acid can induce >> yes is acid B6 deficiency and B6 toxicity also can produce neuropathy.
Usually a neuronopathy can be seen with uh B6 toxicity.
>> Okay sir.
>> Yes. What are the other drugs that other antibiotics that can cause neuropathy?
>> Sir um uh >> uh imipen mainly metronizol linosolid.
Okay sir.
>> Yes. All these antibiotics and other chemotherapic agents like cisplatin vincoplatin. Okay sir.
containing all these things can produce neuropathy.
>> Okay sir.
>> They all produce a symptom like this symmetrical dissel sensory uh motor neuropathy that is of length dependent pattern.
>> Okay sir.
>> Uh so what about this this palpitations?
What do you want to infer from the palpitations?
>> Uh sir this palpitations I would like to uh rule out autonomic dysfunction in case of a gileian bar syndrome sir. uh or uh it could um also be s mostly like uh and any autonomic neuropathy sir other cause of autonomic neuropathy also can cause palpitation sir.
>> What are the other things that can cause autonomic neuropathy? Uh sir in a young female I would also like to roll out hereditary sensory autonomic neuropathy uh HSN but usually presents with ulcers multiple ulcers and all these things will be there sensory uh symptoms will be more predominant not like this.
>> Okay sir. uh autonomic predominant mainly diabetes vin and organopasporus other than GBS autonomic involvement will be prominent uh in drug induced win Christian and argonoposphorus compounds >> yes >> so here the abdominal pain mainly for acute intermittent perferia and arsenic poisoning poison Is this the patient had only blurring of vision?
No dipopia or visual loss. Is he able to uh see see objects? Well, what about the bluring of vision?
>> Sir, uh what she said was she was feeling a blurring of vision uh she was feeling her vision was blurred. But even after uh closing uh right eye and left eye, there was no improvement in vision.
And she also said that she didn't have any difficulty in reading books. And uh she was also able to appreciate colors in the book sir. So u uh we were in like the history is not clear about the visual loss sir.
>> Visual visual loss means that uh involvement of optic nerve is unlikely.
>> Yes sir.
>> Yes. Okay. Continue sir. Coming to past history there is no history of similar complaints in the past. No history of familar fever, abdominal pain, diarrhea for the past one month. Patient is a non case of hypothyroidism on for the past seven years on tap thyroids and 50 mics. And there is no history of any surgeries in the past menstrual history uh uh regular personally.
>> What made just just what made to ask these about these infections the past history?
Why did you ask this? What is the relevance? Actually um the patient is having an ascending parot any preceding history of loose stools which would which could indicate campellobacttor jen that is a pre precipitating factor for for gillian bar syndrome since the patient is having ascending paralysis and no history of surgeries in the past because um history if the patient was having poor ferraria she could have presented with multiple episodes of acute abdomen which could very well mistaken could be mistaken for appendicitis and could have done any appendicctomy in the past. So I wanted to rule out that sir that's why I asked history of surgeries and history of abdominal pain fever and Ira in the past.
>> Okay. Okay. Okay.
>> Okay. What what about hypothyroidism?
Any hypothyroidism in relation to this patient's complaints quadripes and hypothyroidism? Can it be related to hypothyroid myopathy?
>> It could very well be a case of thyroid sir. But in thyroid myopathy it is more of a proximal more than of a distal weakness. More than that in all myopathy, neuromuscular junction and and diseases there won't be any sensory symptoms at all.
>> Sensory symptoms. Okay.
>> This patient has got before the onset of weakness itself, she had some sensory symptoms in all four limbs.
>> Yes sir.
>> So this rules out uh pure muscle or neuromuscular junction or anteronal diseases.
>> Okay sir.
>> Even though there is no clearcut sensory loss, the patient is able to tell.
>> Okay sir. Uh so that should be kept as a last differential diagnosis not the predominant differential diagnosis.
>> Okay sir. Thanks.
>> Okay continue.
>> So personal history consumes Smith's diet normal bowel and bladder habits normal sleep pattern not an alcoholic not a smoker. Summarizing the history, an 18year-old female, a known case of hypothyroidism on treatment, presented with acute onset progressive weakness of all four limbs starting distally progressing proximally. The illness initially began with distal upper limb and lower limb weak le weakness and later progressed to in proximal muscles in a span of six days and she also had complain of blurring of vision without diplopia and without any pain on extracular movements without color vision impairment. Though she complained of napeness she was able to perceive clothes and able to appreciate hot and cold. Though she complained of blurring of vision she was able to read and was able to appreciate colors sir.
So based on this summary what uh did you think about this case? This >> sir uh so far this patient presented with acute onset ascending paralysis sir. So uh and since this patient complained of blurring of vision uh and eye involvement I would first try to rule out enomospectrum disorders sir.
after NMOS spectrum disorders. Uh I would like to uh localize this lesion to vententral motor root sir. Ventral motor root and uh I vententral motor root enospect disorders and uh uh since this patient complains of sensory uh level symptoms I mean both sensory and motor symptoms I would also like to rule out a uh cervical code pathology sir.
Okay. Okay. The patient had three symptoms, isn't it? And uh put the summary slide.
>> Okay sir.
>> Uh so so quadricaris involving all four involving both distal and proximal muscles.
>> So if you take only quadripis the lesion can be anywhere in the neck.
>> Yes sir.
>> Isn't it? Uh only if you take quadripis alone. The second thing >> so I I would say so if we just take precious alone we can localize to anterior horn cell ventral root >> and muscle sir >> muscle uh everything can be there and also in the cord cervical spinal cord >> cervical yes sir >> okay so the second symptom is blurring of vision only three things it is written there one one is progressive weakness other is blurring of vision blurring of vision what do we want to account Two >> sir account two >> sir uh I would like to rule out eno spectrum disorders and multiple sclerosis sir patient is not is not having any pain on eye movement no dipopia and uh there is no clearcut visual loss isn't it she had only picture okay this may be maybe due to involvement of optic nerve or it may be due there may not be involvement of optic nerve plus or minus we can have it oh yes sir yes sir >> okay that complaint of numbness how where you are going to localizer.
>> Uh sir, actually >> she was able to perceive the hot and cold sensation and also perceive the clothes.
>> Yes sir. Uh sir it could be a length dependent if the patient complain like of complain that of a length dependent neuropathy sir. So vitamin D vital deficiency can be kept as a close differential for this. Ah yes yes that can also be kept as a close differential. Okay. That uh that you you attribute it until neuropathy, isn't it?
>> Yes sir.
>> Yes. Yes. Yes.
>> Hello sir. Sir. Yes sir.
>> Ah yes yes.
>> Hello sir. Hello.
>> Ah yes yes sir.
>> You're able to hear me.
>> Can I continue sir? Yes sir. Yes I can hear you sir. Marip sir. Sir do you want to add anything sir? No sir. Let me continue. Can you hear me sir?
>> Yes sir. Very able to hear you sir.
>> Ju just a few more points sir. Um see first you said patient had difficulty in holding the pen and then difficulty in writing.
>> Uh yes sir.
>> Is it an element or an element?
>> Uh sir uh that is element sir. It's more towards an element. Dist muscle weakness. It's more element.
>> An element.
>> Uh sir sir could be both. I mean sir actually why because this patient had initially difficulty in gripping of the slipper sir but she had uh she was able to insinuate her leg into the slippers sir. So this distal weakness more favoring element than sir.
>> So how will you differentiate from an um from an element? uh sir in um the patient will be able to the patient will have uh uh inn weakness the patient will be u able to uh do uh things I mean the uh involvement will be um sir the patient will in also you'll be having only dist weakness weakness okay sir what made you to think in terms of only uh element element Sir um sir that when she arrived at our hospital she was she was carried by two people sir and she was only able to walk with the help of two people and she wasn't able to >> the weakness whether it is a fly type of weakness or a stiff weakness >> sir [laughter] weakness weakness that will differentiate you whether it is or element >> element okay sir >> so it's a fl weakness >> fl weakness >> so what are uh muscles involved in holding the pen.
>> Uh sir the palmer uh sir holding the pen uh uh the adductor policis longest adductor policis brievis and the lumbricals of the first uh the lumbricals of the first uh metacarpal joint and uh and palmer adductus and dorsal and uh dorsal indro vententral inroises. No known it like this much you can say the intrinsic muscles of hand >> the thinner muscles and the muscles >> flex muscles of the thumb and the index finger.
>> Okay sir.
>> So a simple way to differentiate between a new and element. So in case of lower limb so when a patient has difficulty in insinuation difficulty in holding the slippers and difficulty in removing the slippers. So these three is present it's predominantly a human.
>> Okay sir. So in case of an element the patient has is able to insinuate but has difficulty in holding the slippers.
>> Yes sir is able to easily remove his slippers.
So this get an element.
>> Okay sir.
>> So with this you can differentiate an human from an element. So similar way in the upper limb >> the patient is able to take the pen.
>> Patient is able to hold the pen and the patient is able to release. So these three things you have to look for. So in this you said the patient has difficulty in holding as well as difficulty in writing.
>> Yes sir.
>> So this comes predominantly as an element.
>> Yes sir.
>> In human the patient will have difficulty in uh taking the pen, difficulty in holding the pen as well as all movements will be difficult.
>> Difficulty. Okay.
>> Element the holding alone and then writing alone will be difficult.
>> Okay sir.
>> So this will differentiate on human from element.
>> Thank you sir. The why this elemention because there's the weakness of the intrinsic muscles of the hand predominantly the uh thinner muscles plus the first two lumbricals as well as the uh opponent's muscles.
>> Okay sir.
>> Yeah you can proceed.
>> Thank you >> sir. Coming to uh general examination general physical examination. Patient is conscious, oriented, ephemerra, wellbuilt and nourished. Pal present neck. There was a neck swelling and wasting of hypoththear muscles on examination. No neurocitinis marcus seen no mark no short no down hairline and actually kyphosis scoliosis were unable to be appreciated because the patient was unable to stand.
Uh so this was the uh palmer I mean uh cloing of the hand which was and wasting of both hypoththear and thinner muscles.
The the wasting is not that visualized but this is the cloing uh that was present in the patient.
>> So this indicates predominantly a fl weakness >> fl weakness. Okay sir sir. Uh coming to vitals uh pulse rate 78 beats per minute regular rhythm normal volume no vessel wall thickening felt in all peripheral pulses no radio or radal delay blood pressure 110 measured in right upper limb in super position couldn't be measured as the patient was unable saturation 97% under Fahrenheit systemic examination TVS S1 has to hurt RS bilateral entry present per abdomen and soft coming to cranial central nervous system examination higher mental function patient was conscious oriented to time place and person memory both um intact short-term reason and remote memory patient is a right-handed individual speech was uh normal normal comprehension normal fluency and normal repetition coming to cranial nerve examination all factory examination was normal Normal optic now visual acute was 6 by6 on both eyes color vision was normal funoscopic examination was normal ok motor no I mean 3 46 extra move mments were intact trimminal sensation of face normal able to cleanse the teeth cornal and conjunctive reflexes were present facial nerve wrinkling of forehead intact tight closure of the eyelid present nasol labial fold present t sensation the antit of the tongue intact uh vestibular coar now both reneers Those were done. Air conduction, B and B bone conduction and on Webers heard equally on both sides. Cran 9 10 11 UI in the midline and gag reflecting gag reflex back. Spinal ancestry nerve able to shrug the shoulders against resistance. Able to turn head against resistant hypoglossal nerve no deviation of tongue proion. No faciciculation.
Spine and crania no spinal tenderness.
Kyphosis couldn't and scoliosis couldn't be assessed because of the patient's inability to stand. Motor system examination. Antitude patient in supine position. Bilateral upper limb on by the side of the patient. Bilateral hip in neutral position. Bilateral knee joint in neutral position. Motor bulk arm, forearm, thigh, leg symmetrical. Tone upper limb both normal and right and bilaterally normal tone. Power 3x5 uh uh 3x5 uh power on shoulder uh elbow 2x 5 and wrist 2x 5 in f wrist flexion and extension elbow flexion and extension 2x five shoulder adduction abduction flexion extension internal external rotation all 3x 5 sir coming to power and lower limb hip flexion extension 3x 5 internal rotation external rotation also 3x 5 knee flexion extension 2x5 ankle dosive reflection, planter flexion 2x5.
Superficial reflexes, coral reflex present, conjunal reflex present, abdominal reflexes were absent, plantar reflex uh flexer, jaws normal. Coming to deep tendon reflexes, biceps reflex was exaggerated. Three plus on both uh both sides. Triceps uh three plus on both sides. Superated two plus on both sides.
Finger flexion one plus on both sides.
Knee knee three plus on both sides. an angle check one plus on both sides. So this here uh this is the reflex that has been elicited triceps reflex.
>> See uh just normally if you suspect GBS uh just can you hear me?
>> Yes sir sir I can hear you sir.
>> You suspect GBS what is the first reflexes which you will lose that GBS?
Uh sir uh angle reflex uh then followed by uh angle reflex supenator reflex followed by uh biceps and triceps.
>> Yes. Why anchor reflex is affected first?
>> Uh uh sir uh I'm not sure about the reason sir.
>> Okay. Okay. Okay. It's a longest. So that it is lose to loosen GBS. Okay.
>> Okay. Thank you. So angle reflex anything like reflex gap you know about it.
Uh yes sir uh I am not sure >> particularly in early GPS you can note it because usually in GPS we don't have reflexes but here uh you have with the retained reflexes that is reflexes gap anything called as reflex gap have you tested for it >> sir actually the in certain patients the reflexes starts losing uh after three or four days of the pro uh onset of the disease. Actually the nad of uh the disease can happen from 12 days to uh 12 hours to uh 24 days sir.
>> Okay. See reflex gap what it means is it is a preserved upper limb reflexes actually upper reflexes like biceps and triceps will be preserved whereas you can have an absent or reduced ankle js comparatively.
>> Okay sir. And sometimes it is suggestive of an early GPS involvement. You can have it later only you'll have lost reflexes. Reflexes lost. So you should know that reflexes gap.
>> This patient is also having the same type. It seems the patient's uh ankle reflexes are low but brisk knee reflexes and upper limb reflexes.
>> Yes sir. Yes sir.
>> Yes. Correct.
>> Sir.
>> Okay. Just >> video playing sir. Video is not playing.
>> Try to adjust.
>> Not playing as sir.
>> Okay. You say what is happening there.
You don't have to play.
>> Okay sir. Actually what happens is the patient is having an exaggerated uh triceps reflex exaggerated knee reflex.
Uh so um this was that the video is not playing sir. Sorry for the inconvenience.
So coming to uh sensory system examination sir. U sensory system examination. C uh C4 dermatome pain, temperature and fine touch, crude touch all the four sensations primary sensations were indexed in C4 C5, C6, C7, C8, T1 level.
Coming to thoracic level in T2, T3, T4, T5 all the thoracic segments also both all primary all the primary sensation including fine touch, crude touch, pain and temperature were normal. Uh in L1, L2, L3, L4, L5 all on the lumbar dermatomes also all the primary sensations were intact sir.
uh uh s uh rober sign could not be elicited since the patient was unable to stand. Cortical sensation, normal tactile sensation and twooint discrimination and serial is present in this patient. Sir uh cerebilar function sir actually the patient was able to do the finger nose finger test but it she had some difficulties because of the weakness. uh heel shin test also actually uh she was able to do but with difficulty because of the weaknesses no nestagmas no intentional t no titubation tandem walking couldn't be done gate couldn't be assessed uh the length from the oipit to C7 was 12 cm but height to neck ratio couldn't be assessed because uh the her inability to stand so summarizing so far an 18year-old female a known In case of hypother just just have you done any autonomic function testing particularly for this patient >> sir we were actually wanted to do uh postal check wanted to check for postal hypotension sir but since he wasn't able to stand couldn't do sir >> sir what if you would have observed for postal hypertension what would be the finding here >> uh sir autonomic dysfunction is there what is an inference for Uh sir uh if the patient is having an autonomic dysfunction in this patient who is having an ascending symmetrical pure motor paralysis with early loss of angle reflex I would suspect uh a uh gillian bar syndrome with autonomic dysfunction and this patient actually requires ICU care rather than a w care sir because since she's having autonomic dis >> just it need not be always standing. You can also ask the patient to sit from a lying down position. That is also an app.
>> Also an you have to measure both the heart rate and BP whether it is variable or not. What is a drop in the BP is there. If it is greater than 20 mm or systolic or greater than 10 mm >> then our resting heart rate that is a variable heart rate you have to think of early autonomic dysfunction which can be uh if you suspect GPS it should be uh taken care that is very much important >> in the patient always because you are you have done the reflexes testing in the uh sitting portion that portion is enough just lying down if at all not able to stand you can go for it Okay.
>> Okay sir. Thank you sir.
>> Okay. Have you done examination? Pupil examination any finding in the pupils?
>> Sir pupil is bilaterally reactive to light. There was no finding in the pupils and funoscopic examination was also normal.
>> Based on the pupil can you say any differential diagnosis? If the pupil is normal, if the pupil is having dilated or not reacting to light, anything else you can suggest as a differential diagnosis for this case?
Um sir if the patient is having pupilary involvement with uh uh like if the patient is having a pupil spar in third paly along with uh no sir I'm not >> how will be the pupils and gbs just >> sir in uh sir in gillian bar syndrome pupils will be normal and will be reacting to light >> normal normal normal but if at all the patient is having a melia variant what will happen >> sir there will be of themia, a reflexia.
>> Yeah, ofoplegia and a reflexia. But here also the pupils will be spared.
>> Spared.
>> All you have such patients with dilated pupils you have to think of balism also.
>> Okay sir. Okay sir.
>> Go for go for the >> sir. My provisional diagnosis at this point eno spectrum disorders multiple sclerosis CV gension anomalies and gileian bar syndrome sir >> okay these diagnosis that will uh that will fit when uh when it is with history >> but uh clinical examination patients uh sensory system is normal isn't it?
>> Yes sir. uh completely sensation is normal. No bubble bladder involvement.
Uh from the history it looks like it is a pure motor weakness, isn't it?
>> Yes sir. Yes sir.
>> Uh so pure motor weakness I think these difficulty diagnosis will come down.
>> Okay.
>> After examination uh >> it's after examination. uh the only thing that is against uh the diagnosis of ADP or GM syndrome is the brisk reflexes and the only thing that favors spinal cord dysfunction is also the brisk reflexes.
>> Brisk reflexes.
>> Ah yes yes they should be kept in mind that uh there's a possibility all these three things but uh they will not occur without any track type of sensory loss or bubble bladder disturbances. It's very highly unlikely and no also from the examination.
>> Okay sir.
>> Okay. My my first possibility will be uh goldenberry syndrome because it is a pure motor weakness with uh either disorder or exaggerated reflexes.
Other things will should come next.
>> Okay. Okay. Continue. Uh >> okay sir. Okay sir. Thanks.
Any word about >> coming to the sir just when you have sir paris >> sir in tick paralysis uh there will be autonomic dysfunction as well sir and also uh the patient can have uh severe autonomic dysfunction along with signs of anaphylaxis.
So in tick paralysis then um his there is no they will also keep classical history of uh any outside travel also sir in case of thick paralysis sir.
Yes. Yes. Okay. Proceed. Proceed. Sir, do you want to add anything sir?
>> What type of poisoning commonly results in flax paralysis?
>> Uh sir uh sir OPC organophosphorate poisoning can result in flacid paralysis. Then uh >> any bites.
>> H yes a snake bite can presenting with present with >> snakes.
>> Uh sir neurotoxic snake bite like crate and cobra can present with uh uh descending paralysis. But here it is specialy of cobra bite. Anything?
>> Uh sir in cobra bite it is uh the um the bite side can have necrotic tissue uh necrotic changes. A patient can have a painful tossis.
>> Painful tossis. Okay sir.
>> Painful tossis followed by weakness of the upper limb and lower limb.
>> Ah okay sir.
>> What is the specialty of a crate bite?
>> Sir crate bite there won't be bite side will be clean sir. Patient will be having and there won't be any response to atropin and neostigment in case of crate bite s. Okay.
>> But in cobra bite there will be excellent response to atropin neostigment. And crate bite also sometimes have a delayed recovery as compared to cobra bite s and requires prolonged intubation sir. Yeah. Then another one special crate b can have a significant abdominal pain also.
>> Okay sir. Okay sir.
>> Sir uh.
>> Oh in this abdominal pain can come with snake bite acute intermittent period and also arsenic poisoning. All these things can present with abdominal pain and weakness of all volumes.
>> Okay sir. Thanks sir. Coming to investigations. uh these are the CBC of the patient normal s there is nothing significant in the CBC of this patient and this is the LFT of the patient LFT was also normal uh coming to thyroid function test normal urine bore firings normal B12 more than 2,000 peripheral smear examination was also normal viral markers uh negative and uh since the patient had brisk reflexes and those she complained of a visual disturbances We first proceeded with an MRI C-span with whole spin screening sir. This is the MRA of the patient which was absolutely normal and uh sir are can I sir is the MRA visible sir it's absolutely normal u and this is the MRA brain of the patient and in uh since MS was also a differential we checked for the plaques and there was no plaques in the uh both in the uh spine and the brain we checked uh um and uh aquaporin 4 antibodies were also four antibodies also were taken and it was came as normal s and nerve conduction studies none of the upper limb and lower limb nerves were stimulable sir uh leading to a diagnosis of gillian >> bar both sensory and motor both are not stimulable >> both upper limb lower limb sensory and motor Nurs not simulated. Sorry sir. Type typing error. Sorry.
>> Contrast was taken. Contrast.
>> Yes. Yes sir. Yes sir. Contrast only sir. The brain both are contrast along with contrast. Mhm.
>> In this. What is the significance of contrast? In case of GBS >> sir actually uh um sir in GBS or in multiple sclerosis then late is happening in GBS.
root enhancements. Root root enhancement can be >> very good case of so this is the uh psychological experience and we wanted to rule out any previous occult history of uh BLS as well. oloconal band [laughter] also not found in this patient. ological dissociation taken antiGM1 and antibbody uh [clears throat] uh antiGM and antibbody which are diagnosed with and this was the visual potential of this patient since she complained of which was absolutely normal in this patient answer.
>> So when did you do the CSF? On which day you did the CSF?
>> Sir, actually on the sixth day I mean seventh day of the onset of disease and on the second day of admission sir.
>> So when will the CSF will have a significant value? On which day?
>> Sir after 7 days sir.
>> After 7 days. So which is the most significant in initial days of GBS?
uh sir alinocytological dissociation >> in case of GBS GB significant value >> uh sir in in terms of CSF or in terms of investigation sir >> I'm asking investigations >> investigation sir uh seral I mean uh there will be um uh in no conduction study we can >> no conduction stud on day one >> significant day one itself >> CS the significance gets established by Uh 7 to 10 days.
>> 7 days. Okay sir.
>> Regarding infections also uh this this type of quadropus can occur with limes disease dtheria >> limes disease.
>> So infection should also be kept in mind and also >> sir but in infections albinocytological dissociation won't be there won't be there I'm talking about this because we did CSF even infection suspected also these things should be kept in mind. Okay sir.
Sure sir. Sure sure sir. Thank you sir.
>> Apart from infections HIV lymphoma this also to be kept in mind there won't be alino associations.
>> Okay sir.
proceed uh sir uh so uh after uh uh the provisional diagnosis of amsan variant of gileian bar syndrome we proceeded with the treatment of IVIG set and the patient's weakness improved by 90% with the treatment and during the treatment patient was closely monitored in the HDU uh with serial AGS and uh serial assessment of spontaneous uh single breath counter and she didn't require any mechanical ventilation and patient was discussed after 5 days of uh I mean after 7 days of treatment sir 5 days of IV and 2 days of observation sir >> what is 20 30 40 rule in uh GBS >> sir 20 3040 rule in GBS is used to uh whether the patient requests mechanical ventilation of uh or not sir uh like if the um In inspiratory pressure is more than 30 mm of mercury. First vital capacity.
>> Vital capacity less than 20 ml per kg.
Then inspiratory pressure more than 30 mm of mercury and expiratory pressure more than 40 mm of mercury is >> more negative than 30 more negative than 40. Uh yes.
>> So the reflexes are in this case any >> uh sir there is a concept of central disinhibition sir. So basically uh the reflexes are being controlled by the um uh I mean uh the central nervous system uh uh with the help of reno cells. So wrench cells also receives feedback from the sensory nerve cell. So whenever there is an uh inflammation in the uh whenever there is an inflammation in the sensory nerve this feedback from the sensory to the reo cell is being uh uh not happening sir. So because the inhibition of the show cell is loss because of this disinhibition reflexes could be exaggerated in the initial dysfunction of final inhibitory inter neurons that is the main [clears throat] reason for exaggerated exaggerated reflexes and there may be sparing of only aerence also. Okay sir.
>> Aference where it comes a reference.
>> Uh uh sir in the spinal muscle muscle muscle spindle >> muscle spindle. Okay sir. Um sir in the uh of uh sir from the um sir uh >> sometimes the root edma also can compress the card to some extent and may produce brisk reflex >> tendant to the muscle spindle sir.
>> Okay sir. Thank you sir. So which variant of GBS has preserved reflexes?
Leave this case. Which variant of GBS has preserved reflexes normally?
>> That is flex. Why?
>> Oh the sensory is normal.
>> No no no. So the how the uh conduction take place in and out.
>> So it is alternative conduction. Okay.
>> Sorry. So the impulse jumps from Okay.
>> Okay sir.
>> So in the variant when the uh antibodies predominantly not of when the min is preserved the reflexes can be intact. Oh >> okay sir. Okay sir. Thanks.
Significance of ammon variant with any bacterial infection.
>> Sir campella factor.
>> Yeah. Campa is commonly associated with ammon variant. So campa is commonly observed in which country? You know >> uh uh sir western America?
>> No.
>> No no no it is in Asia.
>> Asia. So in developing countries the commonly observed variant is ammon variant.
>> Okay sir. So which other bacteria causes GBS?
>> Uh sir, coronary bacteria and dtheria.
>> Okay. Then >> uh Sika virus, Westnile virus, >> respiratory virus.
>> Uh respiratory sincere virus, endrovirus.
>> Okay. So the campaign causing a GBS the prognosis is somewhat bad.
>> Respiratory viruses causing GBS. the the prognosis is somewhat good.
>> Okay sir.
>> Yes sir. Ammon ammon is more commonly associated with the clamator gi and amsan is assured with respiratory infections.
>> Okay sir.
>> And covid also can lead on to gps like syndrome.
>> Oh okay sir.
>> S asked other other bacteria you can say myoplasma.
>> Micoplasma >> especially in children.
>> Okay sir.
>> It produces a more demilating type of neuropathy.
>> Okay sir. Regarding viruses, hepatitis C, cytolo, epsinto virus, all these things can uh uh develop GBS. All this infection can lead on to GBS.
>> Okay sir.
>> What about introirus?
Uh sir entrovirus can also precipitate GBS like this inrovirus westnail >> west.
>> So these all predominantly involves the antir.
So what is the significance of antel with the involvement of and cell and the root differentiating between and cell and root?
Sir antilons will be having pure sir antons will be pure motor and there will be more wasting than that of weakness but in case of root there will be dorsal root and ventral root.
So one more significant and cell and dorsal root is pure sensory.
>> So and cell in case of polio there will be a column pattern of involvement of muscles. So predominantly the large collar muscles that is the upper thigh muscles and the upper shoulder muscles will be relatively less affected.
Sir I couldn't hear you sir. Sorry sir.
Hello sir.
>> So in case of and cell involving the polio there will be column type of involvement.
>> Okay sir. Column type. Okay.
>> The large column muscles will be relatively less involved while the small column muscles will be more involved.
>> Okay sir. column pattern of involvement which we won't of GBS >> okay sir >> so the CSF in case of polio >> uh sir CSF uh there will be uh pleocytosis CSF pioytosis will be there sir >> it will be similar >> so what what about the NCS >> so no conduction study will uh sir uh the uh uh conduction velocity will be normal but action potential no it will be normal in case of polio and the EMG will be >> okay EMG will be okay sir >> so these questions can be asked in your exam >> okay sir thank you sir so what is acute what is subacute what is chronic in case of this acute flax Paralous GBS.
>> Uh sir um acute is less than four weeks subject to 8 weeks and chronic is more than 8 weeks.
>> Yes. Progression of weakness. Usually in GBS the symptoms typically reach a clinical by two weeks.
>> But if there is worsening after four weeks means we will call it as subacute.
If if there is worsening after 8 weeks we'll call it as chronic.
>> Chronic. Okay sir.
>> So what are the bad prognosis in case of GPS? What are the markers? One is muscle then autonomic dysfunction neck muscle weakness and also if the patient is having the 20 30 40 rule. If the patient is fitting into 20 30 40 rule, it is also suggestive of bad prognosis s and preceding history of campator jen infection is also bad prognosis.
>> Yeah. One more thing is imbalance.
Hyponetia is also the bad prognosis.
>> Okay sir.
>> Yeah. Excellent.
>> And autonomic dysfunction will be the most common cause of death in TVs than respiratory paralysis.
>> Okay sir.
And uh regarding the diagnostic criteria progressive weakness of more than one limbs with a reflexia that are features required for the diagnosis.
>> Okay sir. Brightness criteria.
>> Ah yes yes.
>> Okay sir.
>> And the progression should be a symmetrical progression over four weeks with mild sensory symptoms and signs and there may be involvement of cranial nerve autonomic dysfunction.
>> Yes.
What are the other variants of GBS?
>> Sir, there are a total of 13 variants.
Aman variant, AMSAN variant, Miller Fisher syndrome. Then >> see when you classify it as by neurohysiological studies it can be demilating or a >> yes sir. The other things are only clinical where their weakness may be there or not.
>> Okay sir. Miller fissure syndrome is one part where there is no weakness.
>> No weakness of reflex and attach then uh fngio cervical brachial variant.
>> Ah yes yes the weakness may be local too focal >> thenial.
>> Ah yes yes it may be bipacial weakness or acute bulbar paly.
>> Okay sir. Then u >> it may present with acute datonomia also. Okay sir. Pan dismant >> following infection. How how long does it take for developing GBS? Uh sir following uh an infection it uh sir four uh two to four weeks sir.
>> Uh it's usually two weeks.
>> Okay sir.
>> And the earliest symptom will be distal paristhesia or what we call it as acroparesthesia.
>> Okay sir.
>> There may be back pain also due to nerve root inflammation.
>> Okay sir.
>> Um >> in case of dtheria it takes around period of 3 to 5 weeks. So >> okay sir >> mere presence of sensory symptoms it itself excludes pure motor disorders like motor neuron disase myopathy or myia grievous.
>> Okay sir >> even though there is no objective sensory loss.
>> Okay sir.
The autonomic manifestations uh can range from cardic arithmas. The patient had palpitations but I think her ECG was normal.
>> ECG was normal sir. ECG was normal.
>> Yes sir. Then maybe level blood pressure also blood pressure may increase or decrease.
>> Okay sir. So uh she so during uh in HD we check their blood pressure like every fourthly sir it was uh always near maintaining between 110 to I mean 100 to 110 sir systolic and diastolic between 80 to 90. Yes. To say neurological orthostatic hypertension, the patient uh should have a fall in systolic BP of more than 20 more than 10 without any increase in um and the blood pressure should be measured after 10 minutes of lying down >> and and within 3 minutes of standing of standing within 3 minutes.
And regarding the antibodies, none of the antibodies are specific to the diagnosis of GBS. Like GB, this patient has got the GM1 and GM3 positives.
>> Yes sir. GM1 and GM3 GQ specific G >> only GQ 1B >> for Miller variant.
>> H for Millerial variant that carries a good connection with Miller syndrome.
All others are not specific for diagnosis of GBS.
>> Okay sir.
>> So apart from this IVIG the other model is a treatment >> plasma services.
>> So how many cycles of plasma processes and how long?
>> Sir uh four >> four to five cycles of plasma process.
Four to five cycles of plasma process and alternate alternate day periods.
since she presented we started the heron IV sir.
>> Yeah.
>> What are the side effects of IVG >> sir? IV can the patient can have aseptic men >> then initially the patient can come of headaches then the patient is an IGA deficient patient he can she can present with anaphylaxis >> then uh then uh >> or sucrossse containing iag sucrossse containing ivag products uh the uh it's taken have hypocalemia sir.
>> It can hyper osmolar acute kidney injury.
>> Okay sir. Okay sir.
>> The most other important complication to IV is thrombboolism from highosity.
>> Okay sir.
>> IG deficiency should be ruled out before starting any patient on IV or IGA deficient IV can be given. Oh >> okay sir.
What about combining the two therapies sir?
>> Sir, uh plasma ferosis can be followed by IVAG sir but never IVAG followed by plasmosis because the administered IVAG will be cleared by plasma ferosis sir.
Yes, there is theoretical thought of clearing of IVHG by plasmospheresis.
>> How many percentage of patients get improve with the three treatment? How long does it uh uh take to for the patient to have improvement?
>> Uh sir, it depends on the variant of Gileian Bar syndrome.
So in ADP Miller Fisher and Aman has good prognosis whereas Samson has will take time for the patient to improve approximately about 60 to 70%age of patients will have improvement with the treatments and uh it will take uh the improvement will be after within one one week of initiation of treatment but in case of AMSA it can take two to three weeks. Sir >> role of steroids in GBS >> sir earlier it was straight sir but it is obsolute sir there is no role for steroids in case of gian mar >> but they indicated in cp okay sir so how will you differentiate element weakness from weakness uh sir in a in an uh element u element weakness and weakness the patient will be able to do gross movements but fine destroy movements will be affected sir but in case of element weakness the patient won't be able to do any movements at all sir then uh in case of by in terms of examination the patient will be having exaggerated reflexes in terms of an um weakness and reduced reflexes in case of an LM weakness. Then plunderer will be extensor in case of a weakness and will be flexer or normal in case of mute in case of a uh >> here this patient is having wasting.
>> Okay sir.
>> But having brisk reflexes.
>> Uh yes sir. Uh so um >> wasting with brisk reflexes. uh you M andD can be kept as a different motoring yesing with the brisk flexes you have >> on the same area it is more point we can take M andd into consideration so motor neuron disease considering her age familial should also be ruled out sir but after treatment her we mean wasting also reduced dramatically sir >> is it significant wasting within one week patient had wasting Sir the actually she had couldn't attribute it to the history sir but she had on examinations >> just why can't it be acute onset CADP >> uh sir acute onset CADP uh wouldn't have responded this well to IVA sir then uh the nerve conduction studies uh in CADP um sensory involvement won't be This severe sir >> CDP is demination. This is mainly of a >> neuropathy latency and conduction velocity will be reduced in case of CADP but in addonal varian the cap will be reduced.
>> Okay. Okay. And uh how how will you differentiate critical illness neuropathy or myopathy from this?
>> Uh sir uh critical illness uh neuropathy and myopathy hap usually happens in the set of setup of an ICU or a patient who has been admitted for prolonged uh period s. So in such patients uh there will be uh wasting as well as in certain uh in certain I mean patients they can there could be mild elevation of creatin as well sir and NCS will be normal case of but in critical neurop minimal changes in case of aal conduction s but not like this in this pattern sir.
Usually an axel neuropathy will occur in critical poly neuropathy. Usually ICU setting in patients with sepsis or multiorgan failure. Oh >> okay sir. Okay sir.
>> Well based on the history how will you differentiate there is whether it is a bortalism or not. Sir in case of balism there will be a descending paralysis rather than an ascending paralysis sir then there will be history of mostly canned food intake in terms of portalism and the patient can have it's episodes of loose tools and also there is no such history in this patient sir >> okay then >> uh then uh it won't sensory symptoms >> uh sensory symptoms also won't be there sir.
>> Okay. My >> grain sir my usually presents with an episode weakness that worsens at the end of the day sir but uh in this patient it was a progressive weakness starting from the first day progressing until the seventh day sir and there will be classicaltosis in terms of myastina gravis which was not seen in this patient sir.
Okay. Okay. Okay.
Could it be a cardion like what he said?
It could be a transverse militus. This case >> sir sir there was no objective sensory finding in this patient. Sir a transverse militus would have definitely have an objective sensory level uh and uh in transverse myitis early bowel and bladder involvement will also would have been there sir.
>> Yes. Yes. And uh there will be a band- like sensation at >> band there will be a track type of sensor loss below a particular level patient will not be feel anything.
>> Yes sir.
>> So finally in a GBS if you have a retained reflexes what will you think of?
>> Uh sir early gileian bar syndrome. Uh >> yes, early GBS or >> um CA I mean acute variant of CADP >> ammon variant >> ammon variant. Okay sir.
>> The closest actually acute neuropathy >> one due to campus but there was no history of diary as said this case.
>> No sir no of diary sir.
>> Okay. Okay okay okay. Okay okay okay.
If the patient has reached the nether after 4 weeks.
You said it should reach within four weeks. If it is after 4 weeks weakness is still progressing for this patient means what do you think of >> CADP sir uh a subacute subacute deminating policy and if it is crossing more more than 8 weeks a chronic inflammatory deminating polyadicopy >> but this case you had a reflexes present you said and did you repeat that reflexes uh throughout about the stay of her stay here.
>> Yes sir. Yes sir. Actually the reflexes started uh uh this was at the time of admission sir but the on at the time of discharge she was having uh actually reduced the reflexes sir the major was one plus and even biceps was also biceps and triceps were biceps was one plus and triceps was also one plus.
Okay. Actually in early GBS if you see the reflexes it will be present but as it time progresses it will disappear. So you have to daily examine it. If it is an external GBS that is particularly aman it may stay for a few days. The reflex will be for a few days.
>> Okay sir. Okay sir.
>> Okay.
Who said is a length dependent neuropathy non-engi? What is the difference between this >> sir? In length dependent neuropathy, the patient classically presents with a glow and stoking pattern of uh neuropathy sir. Whereas in non-length dependent neuropathy they will be having patchy loss of sensation and patchy loss of sensation and length dependent neuropathy is more seen in uh uh long track fibers like uh in terms of um mileinated long track fibers. Whereas in uh uh non-length dependent neuropathy there will be more of loss of pain and temperature rather than uh loss of mileinated fibers.
>> Yeah. Length in length neuropathy when the uh symptoms reaches up to the knee there is involvement of the fingers that is the involvement of the hand. So this is typical of length neuropathy. Long length neuropathy is patchy involvement of nose.
>> Oh okay sir.
>> What is monuritis multip?
>> Okay sir.
Sir mononuritis multiplex is usually seen in terms of vasculitis where the patient presents with multiple >> uh sir multiple uh nerve paly sir like a patient can present with a radial nerve paly along with the sural nerve paly. So multiple nerves affected >> nonontiguous nonigous nerves.
>> Non-ontiguous nonigous >> non symmetrical.
>> Hello.
>> Asymmetrical multiple nonigious asymmetrical >> more than two nos.
>> Uh more than two nos. Okay. Okay.
>> What is the typical example of monolitis multiplex?
Typical example >> leprosy and >> leprosy and vasculitis >> diabetes will be a painful sensory motor neuropathy.
>> Okay sir.
>> Uh the individual peripherals can also be involved with involvement of other organs.
>> Okay sir.
So first there is a motor symptom then sensory so involving both upper limb and lower limb.
>> Yes sir.
>> That is buckling of knees.
>> Uh sir actually she didn't give any proper history of buckling of knee sir.
>> Okay.
>> Uh after fourth day of weakness she said she wasn't a she was able to walk some 3 to 4 m. Then she had to lean toward the wall to continue walking. Sir, it was not like that of buckling of knee. Sir, if it if the history of buckling of knees was there, posterior column uh should have been taken more into consideration.
>> Poster column suddenly posterior column for buckling.
>> Uh sir, because join position since loss of joint pos no. What is painful buckling? What is painless buckling?
Sir, painful buckling is due to uh a painless buckling is due to uh u the patient is I mean the patient's body is unaware of the joint position.
>> So >> yeah painless buckling predominantly occurs in muscle weakness and painful buckling predominantly occurs in ligament and >> ligament. Okay sir. So what are the muscles involved in standing of a >> sir sir in standing there will be extensors of the knee and [clears throat] flexes of the hip that is uh being uh used sir. So uh the extensors of the knee are the quadriceps uh quadriceps femoris.
>> Repeat it once again >> sir. The extensors of the knee and uh uh extenses of the hip. Sir >> extenses of the knee and extenses of the hip >> in uh standing. So it's extenses of the hip include ilios as glute. No no sorry sir. Glutius maximus.
>> Yeah.
>> Uh the for standing the muscles involved are the predominantly the first two muscle comes the spinal muscle. So extensor erect spina.
>> Okay sir.
>> Comes the extensors of the hip predominantly glutius maximus.
>> Glutus maximus.
>> Then the extensors of the knee joint predominantly quadriceps.
>> Quadriceps.
>> Then the dsip plexus of the ankle joint.
>> Okay sir. So predominantly extensor alysis lungus and uh tibialis anterior >> tibialis antior.
>> So in case of buckling these muscles can be involved. So either spine or the maximus or the quadriceps any of the muscles can be involved.
>> Okay sir.
>> What is goasine? Sergo sign is classically seen in basus duchian musculardrophe where the patient has proximal muscle weakness. So the child stands up with the support of the arm uh with the hip extense I mean um the patient st I mean the child stands up with the help of arm supporting to the ground sir because his proximal muscles are weak.
>> Yeah. The keeps the both arm by the side then keeps the both arm towards the both knee joint and then patient extends >> extends with the help of the arm.
>> Yeah. So in this >> he claims on his own body actually to stand up. Okay sir.
>> So how will you differentiate human weakness from weakness?
Uh uh sir in terms of history u if um um in terms of uh history in element weakness the patient won't be able to uh grip her uh chapels but in terms of um weakness the patient won't be able to uh the patient will have difficulty even in incin I mean sorry in terms of element weakness the patient will have difficulty in both insinuating and gripping the chapels but in terms of to um lesion the patient will be able to incinate but will won't be able to grip the chapel sir.
>> See a simple thing if in case of an weakness the legs will be very stiff.
>> Okay sir.
>> The patient can't be able to flex his knee joint or able to dip his ankle joint or extend the extend or flex the hip joint.
>> Okay.
>> Patient should be lifted up.
>> Okay sir. So in case of an element leion even though the weakness is there patient in case of initial state patient will be able to stand on his own.
>> Okay sir later stage patient have difficulty in standing >> standing. Okay sir >> it is based on your history and your examination findings. Okay sir, >> what findings would have pointed towards a periodic paralysis rather than wake GBS?
>> Sir, uh sensory in periodic paralysis there won't be any sensory symptoms sir and there would have been in periodic paralysis there would be definitely a previous history of similar episode in the past sir. So uh and reflexes will also be diminished in terms of period hypocalemic periodic paralysis.
Okay. Then the weakness also it will progress.
>> It should be triggered by either some exercise or >> exercise or a car. Right. Yes sir.
>> Yeah. Then usually it involves legs, arms.
>> Okay.
>> But usually reflexes will be reduced or absent during an attack. During an attack.
>> Okay. uh but definitely the duration will say everything and the recurrence I will say that it is a periodic paralysis.
>> Okay sir will be completely intact as you said.
>> Okay sir thanks.
So it comes as a differential diagnosis for pure finally the pat >> pure mode. Okay sir.
>> Finally the patient recovered completely. What is the power now >> sir? uh the patient recovered to 90% improvements at the now the power >> four four >> actually in a GBS if the patient presents to us early you suspect GBS you do a nerve connection study and CSF analysis if it comes normal or so and you have a reflexes present still you should suspect M1 variant and it should proceed if you again have a high index of suspicion after 7 days because Like Mari doctor said after 7 days only nerve connection study and G CSF analysis will be much more better for you. [clears throat] Okay. Okay sir. Uh any cranial involvement was there in this patient? Uh >> no sir. No sir.
So which kernel is common involved in GBS cr?
>> Uh seven >> CAD predominantly involves the 910 cran >> 910. Okay sir.
>> Sulfactory cr invol in which this is commonly >> u sir calman syndrome will be having congenital anosmia.
>> Okay. Yeah. Refum disease can have >> disease cerebellar atia retinitis pigmentotosa and anosmis. So truth is commonly involved in which type of >> MS multiple sclerosis cranial nerve five can >> then um vasculitis involves fifth cranial nerve >> fifth cran okay sir >> second cranial ner >> uh sir in enos spectrum disorders and multiple sclerosis sir >> so can optic can be n in GBS >> uh sir optic I don't know sir >> so patient When patient has increased amount of protein in the CSF, so we can have a mild form of papadema.
>> Oh okay.
>> So there will be minimal painful movements of the eyes when there is increased protein in the CSF.
>> That may be the reason for the bluring efficiency complainted of >> maybe this case the bluring may be.
>> Okay sir. Okay sir. Thank you sir.
And in GBS it may be a bfacial weakness.
Usually GBS there will be a bilateral lower motor neuron type of seventh LC usually in GBS bilateral element type of facial nc but rarely we have seen cases with unilateral also yes sir >> yes yes we had we had a case with unilateral element facial pc >> unilateral elements >> so there are various presentations but uh the standard is standard but uh the deviation Also you have to know in a case when you're presenting.
>> So in this case the you said the sensory is not there. So but you should have tested the time vibration.
>> So time vibration and dynamic joint sense will point out to a minimal sensory effect in treatment aspect. Yes, IVIG is better or plasma parasis is better?
>> Sir, both are having uh similar efficacy sir. But in certain studies, initial presentation within 7 days IVA is showing some superior pure plasma ferosis sir. But after 7 days it is both both are having equal efficacy s.
>> Yes. Yes. Initially you can try with IVIG. If it is not responding then you can switch out to plasma ferism but both have similar efficacy but uh days is more >> only the availability cost and contra indications for IVG renal failure we cannot start the patient on IV >> okay >> patient with cardiac problem don't go for pass yes sir mutuman and marupa just uh final wording about this presentation And what is the take-h home messages for all the students based on this case?
>> See here the patient presented with quadripises even though uh the patient had sensory symptoms he was not having any sensory findings. The only thing is the patient had brisk reflexes which made us to think in terms of a cord leion initially and proceed with MR brain and other investigations. Once the M brain comes as negative we proceeded with conduction. That should not be the thing we should do if we strongly suspect the clinical examation does not show any sensory findings it's better to go for conduction uh initially itself.
>> Yes. Yes.
>> When I saw this history before when I read the history I thought it was predominantly card involvement. So >> yes [laughter] in the strongly suspecting card involvement sir >> then once I go through the exam >> see the the red flag sign is if you suspect GBS and if you have a reflexes also we should not delay the NCS we have to go for NCS and see what is the thing actually NCSB >> because this case has proved it actually >> so NCSB you can get a finding on the first itself sir it It will take >> fine 7 days. So NCS on day one itself we can come to a diagnosis.
>> So it is better you can go for NCS because better prognosis you can give for the patients.
>> If treatment is started early the prognosis will be better.
>> Yes sir m >> the red flag actually any final points.
Yes sir. Yes sir.
Red flag suggesting a diagnosis other than GBS is severe respiratory dysfunction without any limb weakness or slow progression early bowel and bladder involvement and severe sensory findings and marked persistent weakness persistent asymmetric weakness usually will be symmetric weakness and also fever at the onset of weakness. All these things we have to think of some other diagnosis other than GPS.
>> Fine. You have to rule out also.
Yes. Okay. [snorts] Do you want to add anything this presentation?
>> Fine sir. Fine sir. Okay. Uh just uh you have done a good presentation and uh based on your findings many of the things you have ruled out that is a fine things. And finally the proof of coding is the improvement of the patient as shown. So clinical examination history and finally investigations all together we have to come to a conclusion so that we have to give a best prognosis to the patient. She is young girl she has recovered very well. 90% of weakness she has recovered that is a fine thing.
Anyway uh we have to think in mind in only looking at reflexes and thinking at correlations we should not be there. So the learning point is that NCS is a must in such cases in the early stage itself.
Fine and it is a good presentation and sir sir.
>> Yes sir. It was nice discussion on the important aspects of practical aspects of history as well as examination especially the touching upon the points related to cervical cord disease versus the demalination disorder and uh both the neurologist as well as you touched upon the other important aspects of differentials also and the different types of GBS also be discussed and more importantly therapeutics really appreciate GG for nice presentation. I think correctly spelling your name. Sir J sir J I S sir >> sir GC sorry sorry sorry nicely presented and he was able to almost answer almost all the questions few questions he was not able to answer that's a basic idea of this type of platform to have exposure for this type of different varieties of questions related to the same problem would have seen lot of code repairs patient but probably would not have exposed this type of questions makes you to understand the need for exposure different types of questions as well.
>> Really appreciate Dizzy for this presentation and encourage your other colleagues of postgraduates also to prepare well and come for the presentation.
>> Yes sir.
>> That makes your understanding much better and answering also that gives you more encouraging what mood for you to present more and more.
>> Okay.
>> This a basic idea.
>> Thank you. I really thank Dr. Narajan sir for coordinating the complete work and really thank Dr. Mari sir mutar sir for nice inputs on the important common problem which the postgrad is going to come across in the examination the quadripesis which can be any type so which is discussed in detail about the differentials of the cord paracis patient. Thank you all the team members and good night all of you. Thank you.
>> Thank you sir.
>> Thank you sir.
>> Thank you very much sir. Thank you.
Thank you. Thank you.
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