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Right. Uh Can y'all see this s lights? Can I reply to my message in the chat? OK. Then you guys uh let's start the session. So today, our topic will be on about uh Gu guillain-barre syndrome that uh guillain-barre syndrome. So this uh before moving on, talking about Guillain Barre syndrome, I would like to talk about this uh cerebral pathways uh involving our nervous system. So sorry. OK. This point. So as we can see uh Guillen Barre syndrome uh in in our system, we have multiple pathways involved in our system. So I would like to talk about this uh uh this uh upper motor neuron and lower motor neurons in our nerve system. So, in the upper motor neurons, this upper motor neurons are uh these neurons which come from our celeb uh cerebral cortex that is from our brain area all the way until the spinal cord. So, uh for example, when I take this corticospinal tract, the first spin, this first spinal pathway, it comes from the cerebral cortex and it crosses in the medulla uh as the cortical spinal tract crosses the medulla and comes to the anterior horn of the spinal cord. And from there another uh neuron, it synapses with another neuro, another nucleus from here and from here starts the second or neuron. So, as we can see, there are two neurons involved this cortical spinal tract. So with this, we can see anything that starts from the spinal cord uh up to the muscle or the sensory organ that is called a lo uh that is called a se second order. So this uh upper motor neuron, lower motor neuron is involved for the first uh motor pathway tract. So, cortical spinal tract is uh motor pathway tract. So this pa part starts as I mentioned from the cortex, the uh anterior horn and spinal cord and towards the muscle. So here, the upper motor neuron is this cortical spinal tract. And the lower motor neuron is a neuron starting from this anterior horn all the way to the muscle. So, the defect in a lower motor neuron, it can be for a, a defect in the muscle itself or the neuromuscular junction, there is a connection between the muscle and the nerve or can be damaged the peripheral nerve itself or it can be damage to the spinal cord here where the nerve starts. So any damage from here to the muscle that is low motor neuron. Now, any damage to the nerve from the cortex, from this or from the spinal cord towards the cortex, any damage in any of this area, it gives you upper motor neuron lesion. So, there are two types of lesions involved. Uh upper motor neuron lesion and lower motor neuron lesion. Now give uh a small comparison when you compare uh upper motor neuron lesion uh with a lower motor neuron lesion. Now, upper motor neuron lesion, when uh damage, uh as I mentioned earlier, when damage occur, occurs to the central pathway, there will be increased tone to the muscle, uh which that provides and there's increased reflexes in that areas. And there's a Cronus present and uh this extensor plant. And when you stroke the plant, uh the sole of a of this up motor neuron lesion, there will be extensor response, that is this response. So that will be found only in upper motor neuron lesion. And there is no fasciculation that is the twitching or significant contraction muscles or wasting. And there is uh more dis there in to move the mu compare to the power loss, which can be found in low, more neuron. So, in another characteristic features of low motor neuron lesion, we have a decreased tone uh and there's decreased, absent reflexes, absent clonus, the plantar are no, no, mostly normal and they can be waste in this uh wasting. Uh wasting and decreased tone of these muscles are very particular, very important ration. We can see wasting that you can see like uh flattening uh at uh flattening of these muscles which uh as because of this use, they can undergo wasting. And also we can see fasciculation that is twitching, a rapid uh muscle contractions can be seen in these affected areas. So this will be a comparison of uh upper motor neuron lesion and uh uh lower motor neural lesion. So, moving on, now, we talk about specific uh guillain-barre syndrome and the Guillain Barre syndrome. There are multiple forms of guillain-barre syndrome or this Guillain Barre syndrome itself is a spectrum of disorders together. So, in this, we uh again, most the two most common forms. Founding Guillen Barre snd is the acute inflamated poly radicular neuropathy and also the acute mo axonal neuropathy. So, these are the most common forms from these common forms. Uh This session, we mostly talk about the acute inflating uh poly neuropathy, which is the most common form found. Uh comparing this is the most common form found. Now this uh we talk about a ID P. Uh it is a uh commonly it is a post infectious disorder. That means uh as I mentioned this uh slide, a patient can have a, a patient can have infection such as a G I tract infection or upper respiratory infection about three weeks before this uh G when they, before his A IP uh syndrome starts. So, in these causes uh camp which causes diarrhea, uh commonly is the commonest organism. Uh the bacteria which causes uh which can further after three weeks can lead to this guillain-barre syndrome. Other causes of this uh Guillainbarre, we have cytomegalovirus viruses, mycoplasma pneumonia or Hemophilus in sorry for this type here. Uh Hemophilus in is why she come there and other causes. Uh in this articles, when you read, you can see vaccinations, swine flu vaccines and rabies vaccine prepare for infected brain tissue has been, has shown it can lead to guillain-barre in some papers and some surgical procedures and trauma has reported because the development of Guillain Barre but these are still uh under case reports. So there's no pro it's not proven in multiple places. Moving on. Now, we talk about the pathogenesis how uh this uh guillainbarre occur. This guillain-barre is a autoimmune. It's an uh well, it's an auto immune reaction. So initially after this infection, these antigen presenting cells, these uh macrophages when they present the uh bacterial antigens to this TMB lymphocytes of the immune system, the B cells convert to plasma cells and they secrete antibodies against antigens. No, no, these antibodies cross uh these uh antibodies which are formed against these antigens by this molecule mimic the molecule mimicry is when these antigens which are found only in this camp, they have a similar structure or they, these antibodies detect these antigens which are, which are similar to the uh myelin ganglia found in uh now uh the nerves in our body. So uh antibodies uh cross track with these myelin ganglioside and they cause demyelination of this. So there can be demyelination of nerve roots and Perner. So as I mentioned earlier that this is demyelination of the nerve roots and Perner, this is a lower motor neural lesion because it occurs after the uh spinal cord. So it is a demyelination of the nerve roots and per nerve. Now, this uh when we talk about my, my uh my, it is uh used for with my action of myelin, it uh increases the conduction velocity of impulses that is found in the body uh found in the nerve system. So it increases the velocity of con uh conduction, increases conduction velocity. So these antibodies will cause destruction mild in the nerve cells. So the uh nerve system is affected after some time, this myelin regional repair itself. So this uh disease which will uh as I which I will talk about more increases and uh maintains and then it comes back to normal status. So, moving on. Now, when you talk about the clinical features of uh guillain-barre syndrome, now, the first symptoms, initially where the patient presents is they have pain numbness and parasthesia, parasthesia, altered sensation, they can feel like a burning sensation or uh numbness, sensation, numbness, altered sensation. So, these are the initial symptoms the patient presents with. Now, when you talk about the pain, the pain is severe in the shoulder girdle area, the back uh buttock and the thigh areas which even the slightest ness we can get. This pain does if the pain is aching or throbbing uh type of pain. Uh After this, it rapidly progresses, that is within days because an acute condition which uh acute uh within a few days, it progresses, it progresses bilaterally and symmetrically with weakness of the lower limbs. And then from the lower limbs, it comes to the upper limbs and from the upper limbs, it can affect the cranial nerves in the cranial nerves. It can affect the third nerve, fourth nerve, sixth nerve causing og or it can affect the seventh ran, giving a low, more uh it's a low motor neuron type. I, as I mentioned earlier, this is a low motor neuron type. So it gives you a low motor neuron type of facial nerve palsy. So this type of uh the, this type of uh paralysis, it is called ascending paralysis. This is because the weakness, weakness comes from the lower limbs and then comes to the upper limbs and then the cran from the lower part of the body to the upper part of the body it affects. So now we'll talk about uh like uh I would like to do you have a question? So I would have, I have mentioned a pole there. Uh If I can see that, I would like to like you all to answer that question too. I give you two minutes. The answer for this question was uh Lyme disease uh uh ion or this C botulism. This uh both organisms. It causes a, a descending type of paralysis where Lyme disease only causes a ascending type of paralysis like uh is Guillem Barre syndrome. So, descending type paralysis affects the upper limbs or the head first and then from there goes to the lower limbs. Ok. Uh Thank you for answering the question, Paul. Now, moving on with this uh clinical features of the Guillainbarre syndrome. So after this paralysis, there can be a global a reflex that can occur. So there's a uh loss of reflexes of the knee jerk, reflex, ankle jerk, uh reflexes, all those uh reflexes of the lower limbs, the upper limbs, all those reflexes may be lost with this low. As I mentioned earlier, a low motor neuron, palsy, it causes a loss of reflexes. So this ache global are reflex that can occur because all the nerves, the nerves, the all the peripheral nerves on the lower limbs, up to the cranial nerves, it can be affected. And in this condition, there is no sensory signs available because mostly only mo neurons are affected. So as a specific point, remember here, there are no sensory signs, mostly more neurons are affected. Now, this is uh how the disease progresses. So we can, we can see that uh after around 3 to 4 weeks after the infection, the antibodies developed and from there on the weakness starts and weakness becomes uh weakness, the weakness increases and it becomes maximum at around two weeks after the infection. After the disease starts. And after they gradually re uh recover, this recover, it is due to the regeneration of the myelin fibers. So there'll be a gradual regeneration. And after that, within about uh fo after about 4 to 5 weeks, we can see the patient will uh come back to normal stage. So this occurs in most patients. And uh as you can see the red line here, the presence of these antibodies, there is anti gang antibodies with these are antibodies formed against the myelin. These antibodies peak when the the disease comes to the maximum level. And after it also declines with as the disease becomes normal, uh antibodies levels also declines. So, moving on, we can see uh now we talk about complications of this guillain-barre syndrome. The these complications can kill the patients. So we have respiratory muscle paralysis. So we have the uh diaphragm muscles and the intercostal muscles which are used for respiration, they can become paralyzed uh uh not allowing the patient to breathe properly. And or also there can be autonomic dysfunction because autonomic uh the autonomic system can uh controls the pulse, blood pressure and others are uh vital functions of the body. So these cells can uh dis can uh dysfunctional which can lead to um a severe life-threatening condition for the patient. Now, I would like to talk about the other uh bit about other variants of this uh patient. So, more than 95% of the patients, they have this uh acute inflamma and radical neuropathy so that they present with these classical symptoms I mentioned earlier. So this other 5% of the patients they present with other variants. So that can be a chronic uh form of this A ID P I mentioned earlier. Uh So the, and in that we have this Miller fish variant, the mill fish variant is when the uh condition starts with the cranial ness affected. first. That is we can have plasia or a refex and A and the central nerves, the cranial nerve and the brain and cerebellum, they are affected first. So this is the most common variant uh other than uh the ID P I mentioned earlier. So the other in the rest 5% of the variants, the most common is the mila fish variant. So here there are antibodies formed against the ganglia GQ one B. The. Then we have the regional variance of Guillainbarre syndrome such as the pharyngeal cervical brachial plexus, uh pharyngeal cervical brachial weakness, sorry, the pharyngeal cervical brachial weakness, uh only one leg weakness. But as you can remember, the normal uh variant of the norm A ID P can see I as I mentioned is bilateral symmetrical. So these variants can only one, a particular limb can be affected or the upper part of the neck area and the brachial plexus area can only be affected by other pa other part of P. But this is a rare condition and uh it also follows this ti time course of the A I time cause I mentioned earlier about A ID P where the patient comes to maximum on two weeks and recovers with time. Another variant here, pus uh pan pan autonomy. That is it's a widespread sympathetic and paras that an autonomic failure. But the somatic nerve fibers uh control nerve fibers, they are uh not affected. So this occurs with little weakness or it is it is also very rare. Uh So we don't find patients with this. Uh Now, moving on, uh we talk about the diagnosis of this condition. Now, this uh clinical picture is of acute flexor. Uh Sorry to mention uh sorry, I couldn't mention any acute fla uh acute flaccid paralysis. It is the same as low motor neuron lesion. So, uh as I mentioned earlier, about loss of uh reflexes, fasciculations and uh muscle wasting. So, those same feat features are found in this. So that is an acute flaccid paralysis. This is uh this uh guillainbarre syn produces a typical picture of this low motor neuron lesion. And uh other methods we can use. Uh we can measure antiviral antibacterial antibodies can confirm an association. So when the patient presents with this clinic, typical clinical picture of this lower motor neuron, uh low motor neuron lesion. And when we measure the blood for any antibodies for any bac organisms, we can find an association that is bacterial organism. I mentioned earlier. So we can find an association there. And the main thing uh we do is we can do a nerve conduction study. So this nerve conduction studies, it shows uh there's a reduced conduction velocity. This is because as I mentioned earlier, the myelin fibro myelin which wraps around the nerve conduct of the axons, it is used to increase the conduction velocity. So these antibodies affect this myelin. So the conduction velocity is affected here, decrease in the conduction velocity. So when you do nerve conduction studies, we can find that there is decrease in the velocity. And another examination uh now is we can do a lumbar puncture. This lumbar puncture uh is done usually after the 14 or 10 to 14 days after the disease has started. So this lumbar pu can be used to exclude other causes of this weakness. It can be uh HIV uh or if there's an atypical presentation of the patient where you cannot find the diagnosis. What you can see in this lumbar puncture. Uh in a patient with uh guillain-barre syndrome is we can find the album albi albumin cytology dissociation that is a pro albumin protein and cy cells. So there, there's a protein cell dissociation. We have a normal cell count, uh the W BC and uh other cell counts that is all normal, but there's a very high protein content. So this is the albumin dissociation which is very characteristic for Guillainbarre syndrome. So, we do see uh lumbar CS examination for this uh uh Gilb patient, we can find this dissociation which is a very important point to remember about Guillainbarre syndrome. Now, moving on to management of guillain-barre. Now, management of Guillain Barre can be uh broken down into these specific points. That is we monitor the progression of the disease, prevent and manage any complications. Are the two complications manage? Uh I mentioned earlier, the respiratory depression and dysfunction that should be prevented and managed if it develops and a general care for the patient on a specific therapy if uh needed and rehabilitation. Now, monitoring progression. Now, when you monitor the progression of the disease, as I mentioned earlier, this uh lower motor neuron weakness, that muscle weakness is very prominent. So we can check the muscle power limbs using this MC muscle power scale as I've shown here that grading it is out of five. So we can uh give a score from 0 to 5 for each limbs and uh find the total score and we should also pro monitor. As I mentioned earlier, he also should make uh as I mentioned again, we should always be ready for identify and treat these complications of this respiratory muscle paralysis and auto army dysfunction. Now we talk about uh respiratory muscle paralysis, how to identify uh this disease. Now, in a vi vital capacity, this is the maximum inspiratory volume and exp volume. A patient can do. So that is a normal value is around 75 ml per kg. Now, if the value, if the value comes less than 20 ml per kg, we should admit the patient to ICU or if the ca capacity, if this vital capacity is rapidly declining, we again, we should admit them to the ICU intensive care unit and manage them and we should start ventilating. The patient with that is artificial ventilation. If the, if the level is less, if the value is less than uh 15 m il per kilo. Now, moving on, we can also check the single breath count that if you ask the patient to take a deep breath and hold it and then you count how many, how much the patient can hold the breath for. So a normal individual can hold the breath for more than around 23 to 25. Normal, they can hold it. If this is, if this value is progressive decline, that it's becoming uh 23 24 22 hours, they be become 2018 that you uh immediate a the patient ICU because they, they have uh respirations being affected. Uh Now, we should assess these values every 2 to 4 hours initially when the patient is presenting with these symptoms. And after the patient is stable, we should check them every 6 to 12 hours. We can also check the pulse, uh pulse extremity that is check the oxygen saturation level of the patient and other arterial blood tests can be done if needed and the peak expiratory flow rate, these measurements can be done if needed. And the respirator rate also can be assessed to check uh if needed in the autoimmune dysfunction or to measure autonomic dysfunction. We can measure the pulse rate and the BP, which are very easy to do initially and we should check them initially every 2 to 4 hours. We should assess these two parameters. Now, after the patient goes into the stable face, that the patient is uh able to breathe properly. And these uh patient is uh in a stable, stable uh position. We should measure these parameters is pulse and BP every 6, 12 hours. And a supportive care is given uh with uh and the patient goes in or dysfunction. And if the patient has a se uh a severe severe fluctuation in the pulse and BP rapidly decline, declining or changing rapidly, we should admit them to the IC immediately giving, giving them an ICU care, then moving on uh the next pop point of management in general care. So we should generally get take care of the pain. This is a support measure. So as I mentioned earlier, the patient will have a low motor neuron weakness in the eyes. As the facial muscles are facial muscles are affected. And uh the lacrimal gland, the lacrimal gland is being affected here. So to prevent uh this lacrimal gland which produces uh the tears. So this uh tears to moisturize the cornea. So to prevent corneal ulceration because because of the dry eyes, which we can uh prescribe the patient, uh we can give the patient artificial tears to maintain the uh film and prevents corneal ulceration and to prevent the thromboembolism. That is AD DVT, that is deep vein thrombosis to prevent this thromboembolism forming in the because of there is no movement from the patient. That's all paralysis, right. So with no movement, there can be this uh thromboembolism forming in the lower limbs. So to prevent this, we can give stockings or we can give a heparin management for the patient. And if the that was checking for swallowing dysfunction, uh A G uh check you check the patient with swallowing dysfunction because the oropharyngeal muscles also can be affected. And uh A G tube, uh nasal nasal gastric tube can be inserted if the pa if indicated to uh send the to for foot uh for foot. And also this is uh done also to prevent uh aspiration. As the patient cannot uh swallow anything. They can, they can directly go into the uh trachea. So that also should be uh should be uh checked. And also patients who have proper skin care because uh they can develop this decubi ulcers. This decubi ulcers is pressure, pressure source. So when the patient is lying in the same position for uh a long time period, the patient can develop uh these ulcers in the back area. If the, if the patient is lying in a su position, the patient can uh develop these ulcers in the back uh in the back due to constant pressure in that area. So to prevent that, we should always uh rotate the patient and uh providing uh provide the patient proper skin care. Then the as there's an autonomic dysfunction, there can be bladder and bowel dysfunction. So that can be that's a proper care for this. So if there's bladder dysfunction, we can insert a urinary catheter for the patient. And also I mentioned earlier that this gin causes pain. So we can uh start with uh this pattern with pain uh management. So initially giving this small time uh an analgesic acetaminophen and I say if uh needed and moving on, we can move on to the pain letter. Uh this analgesic Lader. Now talking about uh specific therapy for these patients. That is uh IV immunoglobulins that can be given for the patient. We're starting early. Uh we starting uh starting it earlier. It is better. So it should be given five days. The earlier it starts after you uh start developing the condition. The earlier we give these IV immunoglobulins, it is better for the patient. So there can be better recovery or a faster recovery. It is given for five days for the patient. Another method we can use is plasma exchange. V uh ex uh uh plasma exchange for the patient. Now, this immunoglobulin IV immunoglobulin plasma exchange efficacy is equal. And uh but this IV immunoglobulin it is easy to use compared to plasma exchange. So IV uh this immunoglobulin method is uh more preferred uh specific uh therapy. But it does it, as I mentioned, it reduces the time to recover. Uh it reduces the need for ventilation. So reduces the chance of patient going into respiratory failure and residual disability. Uh And as I mentioned uh here earlier that starting earlier, the better. So it uh it is beneficial for the patient if you start within the first two weeks of one. So after around three weeks, after the after uh after uh the infection and the patient starts developing uh the guillain-barre that is we that is the weakness within two weeks. The patient presents to the hospital giving him ilo it is beneficial for the patient for his faster recovery and reduces the risk of going these complications comparing uh I mean, now we talk about steroid therapy because this is also like an autoimmune reaction because antibodies are affected uh antibodies go and antibodies by zoom these antibodies go and affects myelin. We can talk about uh steroid therapy and all but the action is uh not preferred here. So it is there is no place of steroid therapy in this uh guillain-barre syndrome. Now, finally, not talking about the prognosis of guillain-barre syndrome. Uh We talk about the prognosis around uh 80% 80% completely recover. That is around 70 to 80%. They complete recover or with this minus small small disabilities, but they completely recover. So it has overall better, good prognosis with 80% recovery around 30%. So around 20 to 30% they develop respiratory failure, ok? And in that uh 20 to 30% 5% can die despite intensive care. With the with all the better care, they also can die. And also 65% are able to walk independently as on six months. So this uh GBA, it can drag on for a long time period. Patients have there is cause of patients even dying after months of the carrying. So it can drag on for a long time period. So we should always be, be vigilant and also be ready to uh identify these complications and promptly treat them. And uh uh that's it guys for today. And uh like uh like the