Multiple Sclerosis : Everything you need to know!

a next lecture today is gonna be on demyelinating disease we're gonna start by talking about multiple sclerosis now we have to start what's the definition of multiple sclerosis let's break the word into to multiple that means many sclerosis and marry me in medicine means a lot of scar tissue so the scar tissue forming well how can we form scar tissue inflammation that is the only way we form scar tissue right there's trauma anything that can trigger inflammation infection damage autoimmune disease anything can cause inflammation but the bottom line is whenever we have inflammation that inflammation we eventually to stay roses which is basically fibrosis of the tissue but in this case since we are talking about demyelinating disease d meaning removing myelinating disease in this case what we are doing is removing the myelin sheath that surrounds the neurons in the central nervous system that's pretty bad don't you think yes I think so so now let's talk about the pathology of multiple sclerosis well in this case this is actually a selective demyelinating disease of the central nervous system selective means a picks specific parts of the central nervous system that is going to be affected selectively d myelination off CNS remember the CNS is made out of the brain and the spinal cord which is the TEL but in this case there are multiple multiple focal zones which actually a source of demyelination which are basically plaques inside the central nervous system that are spread around the white matter who wait a minute wait the white matter come from let's review some basic neurology concepts so in the brain this is a brain in the spinal cord remember and we've got the peripheral nerves coming out now in the brain we have gray and white matter the outside of the brain is actually a lot of gray matter which I'm just gonna paint right here but if it took a cross-section of it we're gonna see white matter running down white matter running down as fascicles well what are this great matter the gray matter is actually the cell bodies of neurons really that's very true the cell bodies of neurons that have dendrites see that those are dendrites and this is an Iran with a nuclear it's got initial substance is guy endoplasmic reticulum Golgi body and then through the axon of hillock right there and it runs down a bunch of accents this axon it's the paths that use kind essence to transport neurotransmitter to the bottom of the axon and this axon is gonna fire and release its neurotransmitter it could be a city choline which is usually common the central nervous system could be GABA gamma-aminobutyric acid it could be dopamine norepinephrine anything whatever the axon is carrying it's gonna fire and use it to connect and talk to the next neuron however in order for an action potential to occur which allows a neuron to fire we need these axons to be D to be myelinated now myelin I think of wires right yes in a electrical wire right the reason why we surrounded and insulate them is to prevent loss of neurons like electrons when so when when electricity is passing through a wire you don't want to lose all the electrons on the way through so the faster the electricity can pass through the wire without getting any stops in the way this is how I think of neurons also they have this axons right with this beautiful myelination called myelin sheath and this myelin sheath allows fast super fast action potentials to run through this neurons so that it can communicate as fast as possible however we're talking about selective demodulation of a central nervous system this part of the neuron is was forms the gray matter and the white part that I was talking to you about is the axons they can call them fascicle axons tracts they mean the same thing now those gray matter from the outside of the brain the white matter is now the axons of the neurons now usually the case in the case of multiple sclerosis we've got multiple different sclerosis well in this case we are dealin 18 so this is what we are doing let me erase it demyelination so let's erase a myelin she sheet right and all of his son is you see that I'm removing the sheet one by one and all of a sudden I've demyelinating the neuron what do you think is gonna happen to this neuron when you remove the insulation that surrounds it well it's not going to be able to fire as it used to so therefore the myelination of multiple sclerosis it's strictly strictly restricted to with a white matter which is the axons of the neurons and this affects both the brain and the spinal cord because this accidents run through the brain and also the spinal cord then which makes about what central nervous system and also the peripheral nervous system is affected now the common tracks there are common tracks are actually affected when patients have multiple sclerosis we're going to talk about some of them now some of the tracks that are affected are the pyramidal and the cerebellar pathways pyramidal and cerebellar pathways another pathway that's affected are the medial longitudinal fasciculus pathway and last but not the least is the optic nerve and the post posterior column now in this lecture I'm gonna talk about the medial longitudinal fasciculus pathway known as MLF pathway and I'm going to talk about also the optic nerve and the posterior columns because when I talk about why the patients present with these symptoms you'll be able to understand this better well on the right side of the board I have drawn out the medial longitudinal pathway well this pathway actually doesn't just exist by itself it's actually a very very important pathway for also be able to conduct conjugate gaze what does conjugate gaze now I want you to focus on my eyeball if I tell you to look over there to the right without moving your head what do you do did you see that I'm able to a be ducked my right eye and a deed also a be ducked a deduct like I ducked my left eye you see that now let's try to do that with the left eyeball by looking to this side well if I want to look to this side without moving my head I have to do that now you see what I did my left eye is a bead achtung and my right eye is a deduct in and now I see you there we go how does her body do that that is a very very complicated pathway as simple as it looks it actually requires using the parietal and the frontal field in the cortex we need the medulla the pons the midbrain just to be able to do that so we're going to go over it step by step now in order for us to be able to conduct a right horizontal conjugate gate remember this is horizontal this is vertical remember there are different high muscles in the that control motor movement in the eyes we have lateral rectus muscle right on the lateral side of the face we have medial rectus muscle on the medial aspect right we have inferior rectus muscle we have superior rectus muscle we have superior oblique and inferior oblique in this lecture we're only going to focus on the line directors and their media rector's and that is a very very important concept because how does my I able to conjugate Li look at that side of the of the on the right side without moving my head see I can move my head like that that is my head movement but my eye movement is called a conjugate gate and both eyes actually are moving in the same direction now the neurons in the brain stem which is your pawns midbrain and medulla and the cortex cerebral cortex are very responsible for doing this now horizontal eye movements are having general generated by neurons that are found in the param median Ponty reticular formation that's a big word the para median pontine reticular formation PPR f p PR f PP RF i also called up it's also called the horizontal gaze now I want us to follow this pathway very very closely because the pair immediate reticular formation which is P P RF is actually going to be connected to the neurons in the absence nuke neurons so now let's follow this see we are now inside the pons this is the pons now let's say I want to have a conjugate gauge to the right I just want to be able to look to the right I have to activate the left frontal field because the left frontal field has to cross over into the opposite side of my brain of my brainstem which is the pons to be I'll allow my right side of my eyeballs to actually be able to conduct conjugate horizontal gaze so when you activate the neurons inside the left frontal field they're gonna cause me to have a right horizontal conjugate gaze so when this neurons fire see how one is coming from the left frontal field or okay and the provider cortex they're going to activate the power the right power median pontine reticular formation and that actually synapses with the abducens nucleus now what comes out of the abducens nucleus it's the right abducens nerve now what is the function of the abducens abd look at the word abducens it's pretty word into two sounds like the it's gonna a be duct a b duction and what is one of my a B ducts what do those do it goes to this side it goes to the lateral side when an addict I add to the middle so if I say adduction I'm adding to the middle oops I'm a deduction I'm subtracting from the middle or I'm moving to the lateral side so follow this pathway now the PP RF is gonna activate the neurons inside the absolute abducens nucleus which is not gonna stimulate this up just this nerve which is the right abducens nerve and what do you think is gonna activate with muscles is gonna be a be ducted well think about it if my eyes has to move to this side there's got to be a muscle that's pulling it this direction it's on the lateral side so that is called the lateral rectus muscle lateral rectus muscle inside the eyeball and that is that muscle right there because his job is to pour just my right globe my right eyes towards the right so now I'm if I close my eyes see I'm looking to the right well I'm activating my right lateral rectus but that's being caused by activation of PP RF following that excellent now the PPR F which is we're still right in this area that's the entire PPR F also give rise to axons that course in the medial longitudinal fasciculus MLF which often cross the midline which often cross the midline now let's take a look this is the midline of the midbrain the PP RF is now going to activate the MLF which is the medial longitudinal fasciculus pathway and which is gonna cross over see how he crosses over to the midbrain and what does it synapse with well it's gonna go and synapse with the ocular motor nucleus ah wait a minute the oculomotor nerve well this is the ocular motor nerve the oculomotor nerve which is gonna be the left oculomotor nerve because now we talk about the left side of this remember where you crossed over to the left the left oculomotor nerve is going to activate this muscle hmm this is our nose this is the right side this is the left side this is the medial aspect of the eye so what muscle do you think that's gonna be well that should be the medial rectus muscle which is innervated by the left so that would be the left medial rectus muscles which is innervated by the left oculomotor nerve now what does the medial rectus mostly do well it pulls my eye in towards the middle because it's medial so what is the function e ad ducts the ah ad Docs addicts the eye to the middle therefore using the medial longitudinal fasciculus I'm now gonna be able to what a deduct a deduct so it's as you can now see the patient will be able to have a write a B duction by using the lateral rectus muscle and you're also going to be able to deduct that I as you can see when I move my eye without looking without moving my head right my eyes like that and that's like that that is what you seen exactly on the board I'm demonstrating that so that you can see that the MLF which is the medial longitudinal fasciculus is going to the midbrain activating the left oculomotor nerve to activate the left medial rectus nerve which is activating to the left I'm sorry the left medial rectus muscle for us to be able to eat deduct our eyeball and that is how we perform horizontal gaze therefore when we stimulate the PP RF what is the overall summary we get epsilon or sim sight horizontal conjugate gaze by stimulating the PP RF on the right what do we do it results in a reduction of the writer and a deduction of the left eyes but I wonder why I spend all that time just to explain this pathway known as the conjugate eye movement pathway it's because it's very very crucial in our lecture in multiple sclerosis I like to be very detailed now what will happen when a patients develop multiple sclerosis they are going to develop demyelination demyelination of the medial longitudinal fasciculus pathway oh no isn't that MLF yes but there's two of them it's not just one there's actually two of them because I'm just using this to show right horizontal on the left side there's another one that crosses over that will also come down and innovate the medial the medial rectus muscle on the right eye and there will be another left P PRF that we eventually calm down let me use that as green something like this and innovate the latter left lateral rectus muscle so I'm only using one as an example but the reason is because when somebody has multiple sclerosis this is what will happen this is what's about to happen let's use blue they're gonna get demyelination of this medial longitudinal fasciculus right there see that both of them is gonna be a bilateral by lateral because both of them are going to be damaged what will happen when these patients with demanding multiple services disease develop lesions in the MLF pathway they're going to develop a syndrome called intra inter nuclear ophthalmoplegia inter nuclear optimal pleasure pleasure means weakness eye weakness I witness inter nuclear inside the nucleus now let's take a look and explain this what does inter nuclear or family you mean it simply means when I damaged both MLF the patient's now we have a problem with what a deduct in because remember let's look at MLF again MLF goes all the way to the medial rectus muscles so when I tell the patient to look to the right right do this they will be able to a be duct why because the P P arith go straight down through the right abducens nerve enter the lateral rectus muscles to fire contract and move to the right that's good but their left eye will not be able to a deduct why because the MLF is damaged so it's gonna stay in the middle so this patient will be unable to a deduct this eyeball when I tell them to look to the right now let's talk about the left if I tell the patient to look to the left the lateral abducens nerve this one in green will be able to be activated from the PP RF in the pond however their medial which would be this medial rectus muscle will not be able to deduct so this patient we have inability to ad doctor but either I whenever you tell them to be able to have a conjugate gaze however this patient's convergence is going to be intact so when I mean what about convergence what you want to do H in space tells you tell the patient to look up down and go across up down but when you put your eyes in the middle they will be able to converge both eyeballs in because convergence has nothing to do with either medial lateral a medial rectus muscle also these patients suffer been unable to a B duck normally they might have some mono ocular nystagmus when they a be docked in the eye what does that mean mono ocular night nystagmus nystagmus is when you tell the patient I want you to follow my pen and go to the right when I tell it somebody to look to the right that I bought you don't be coming back like this no shouldn't be doing that if you see their eyeball going this way and coming back and try to move it back to the center that's called nystagmus so when the patient has multiple sclerosis they have one single eye we try to go back to the other eye to try to correct it remember this eye is not going to move when I tell them to go to the right because it's going to try to correct it and come back to the middle just one warning if your patients us have just one you're not unilateral ijen you know just one of the MLF it's an infarction it is not not multiple sclerosis it's basically and in fact it's be a schema in the brain it has to be a by lateral now that explains what MLF means when the patient's has multiple sclerosis now if they have it they can have a damage also to the optic nerve right remember the optic nerve is the nerve that goes and supplies the eyeball so we've got the optic nerve which supplies the eyes and it's what try what does optic nerve do it's what carries all the information that's been translated in the retina all the way back to the occiput so they can have damage to that and also last but not the least the posterior columns we haven't talked about posterior columns but we're going to talk about that in a whole different lecture in the posterior column pathway but the posterior comes up is the pathway that run in the posterior aspect of the spinal cord posterior aspect of the spinal cord which involves your touch vibration sense inside the spinal cord and when they have lesion in this pathway then we have sensory loss now the incidence of multiple sclerosis is very low in people that live below the equator so people that live in Africa and also some higher and Africa they do not develop multiple sclerosis so if I drop the world this is the globe right and this is the United States and Canada on top right and we have Brazil and when we have Africa basically people that live above the equator are more susceptible to developing multiple sclerosis compared to the people that actually live below and the incidence just is very high in people that live in this part of the world and also often women by far are 2 to 3 times more likely than men to develop this disease so it's most likely found in women so let's talk about the incidence of the disease above equator higher latitudes and women by for 2 times 2 to 3 times more likely to develop MS they're men what it causes MS what's causing this demyelination what don't happy nice if I knew the answer I don't know the causes are known nobody knows why this demyelinating disease is destroying the neurons axon myelin sheet however they think it's probably a balance between environmental factors some immunologic factors or even genetics but we don't know what actually causes the disease so let's talk about clinical features or what the patients often present with when they have multiple sclerosis patience - MS often start of having transient sensory deficit transient sensory deficit remember the reason why they developing sensory loss which is very short amount of time try that's what trans it means very short amount of time sensory loss it's because the posterior column which are the neurons actually go through the back of the spinal cord and the posterior aspect of that run all the way and of course I can go to the thalamus are actually bendy myelinated that's why they develop this this is how when I start them I feel like oh I feel a little patch here I thought I couldn't just I couldn't feel just this part of my arm or this part of my arm this part of my trunk just feels numb I don't know then it goes away that's usually how you initially start and then they have a lot of fatigue a lot of fatigue that's the most common complaint that I'm always tired then they develop motor symptoms such as weakness weak arms and they know that my arms are always feeling weak or my leg is always giving out of me it's very very weak but and there's our motor symptoms or sometimes they develop spasticity spasticity or weakness well spasticity business is an upper motor neuron disease and whenever you're up on the run upper motor neuron disease you always have have very very stiff muscles and this usually that means an upper motor neuron disease and often it's the pyramidal tract the pyramidal tract is what causes them to often have this kind of acute onset also they might say they have a lot of leg stiffness like I couldn't just move my legs and this prevents the patient's from walking over maintaining their balance because that leg is very very steep and eventually this can lead to weakness and also progression to hemiparesis or paraparesis even quadrupoles because this case is a very very severe diseases these patients also have optic neuritis which causes them to develop visual disturbances let's talk about that visual problems this is from lesion of the optic nerve demyelination of the optic nerve and often this patients complained of mono ocular vision loss and this can happen up to 20% of the time of patients they just say doc I couldn't see my right eye how do you know what happened and also they can help pain when they are moving their eyes around another thing that you can patients can complain is something known as central scotoma what is central scotoma patients report you have dark spots dark spots in the center of their vision and this it's just that I just has just see this dark spot right in the dead center and it's not going away and then when you take the flashlight and the panel I tend to check for the pupillary reflex they might have decreased proper reaction to light and we already talked about ophthalmoplegia which is another science of symptoms which which is actually what strongly suggests the diagnosis my patient have intranuclear ophthalmoplegia you can guarantee yourself that this patient has multiple sclerosis also they can complain of diplopia which is double vision right they have already damaged their optic nerve they might not be able to see very well if the cerebellum is affected cerebellum is the part of the brain that's responsible for balance right that's how maybe to not fall when I'm standing well unfortunately for this patients if they have lesions to the cerebrum what are you gonna have ataxia you're not gonna be able to have good balance and also they can develop intention tremor right intention tremor and which means they try to grab on to something and all of a sudden in their hands is shake and that is intention tremor so you tell them finger to nose and if you try to put their finger you have an intention there intention to do something but it can because cuz they have a lot of tremor that is intention tremor and this pushing can also have this author dysarthria because they can develop upper motor neuron disease become permanent disease conferred in their brain and the spinal cord this can cause them to lose their bowel and bladder loss of bowel and bladder let's erase this so we can get some extra space for this clinical features loss of bowel for number five year Bower and bladder which means they can't hold their bowels they poop on themselves or they can also urinate on themselves because this if they ever damage the motors are this the control center and the brain for the Bower and their bladder or this patients also have autonomic disturbances which can lead to impotence constipation and last but not the least we can develop neuropathic pain and this is very very frustrating but very very common complaint because they develop they can develop trigeminal neuralgia trigeminal neuralgia new Raja or even develop hyperesthesia hyper Cesar the extremely very sensitive to pain to touch and they have trigeminal neuralgia when somebody are generally light touch their face or even a wind blows on their face it causes excruciating burning pain that is charger Madonna Roger and this is called this is neuropathic pain because the nerve pain neuropathic pain and on top of this all this patient can have cerebral in involvement inside the cerebrum and this can cause the patient to have a lot of emotional problems memory loss they start to forget a lot of things you can have personality change their mood changes they develop a lot of anxiety and depression because think about it you start with some part of your body's being funny and feeling numb and then it progresses to motor problems you know they just wake up one morning the leg is stiff they can't walk and also another day they realize oh my goodness I can't see cuz I have visual problems I'm trying to look to the right my Eyes's hack them funny and they can just start to notice they have a loss of bowel and bladder this is a very very debilitating disease especially when they have a lot of excess emissions of the disease and can cause them to also have memory problems they're forgetting things where's my car keys see how this can roll the ball and I affected patients just basically life you know imagine you try to go to work in the morning and you're lucky stiff you can't drive your car that is very the first Radian you get a lot very nervous I got to call my boss I can come in because the disease is affecting their lifestyle and then you get depressed because you know one day they realize oh my goodness you know I have blood via a severe pain and this pain is causing me you know problems and I can't go out alright so how does this disease progress in terms of its course well most patients that have this disease initially starts in their 20s and 30s that's usually when it begins around 20 years old to 30 years old and often they have those are local deficit that I talked about which is the optic neuritis the one-sided weakness numbness of their body but following that they're different variants of multiple sclerosis often that the different variants are it could be clinically silent we're just talking about the course of the disease clinically silent what do we mean by clinically silent well patients this is often those either benign or stable multiple sclerosis often there might be some progression of the disease later on in life and then we have the relapsing and remitting course what does this mean when we say relapse and remain remain off and on that's the Fernan English word on-off on-off so when patients start to have a lot of symptoms whereby they have an excess evasion of the disease right you have this they might say you know what during the winter I get a lot of weakness a lot of numbness a lot you know a lot of blurred vision and it's you lasting for weeks and then as the weather start to change I feel better they're like ah so it was relapse and he came on and during the summer I feel great oh man my mood is good I'm not icky today I'm not pissed off because I don't have any weakness I don't have any blurry vision I don't have any double vision and I've been a pain that means the disease is now repeating that is what we're meeting me so it's exacerbation remission by far this is the most common type of the disease most common form of multiple sclerosis that is usually how most patients often present like this the other form is the progressively worsening or the primary progressive multiple sclerosis or secondary I'm sorry secondary progressive secondary progressive that's another course of multiple sclerosis and which one is this well this is awful with patients with relapsing and remitting disease but it can experience gradual worsening of the symptoms and this is often progressive as a years come down the line that's called secondary progressive but the last one is known as the primary progessive and this often a steady progressive disease we got primary progressive so primary progresses would be like this they're slowly building up slowly building up over the years twenty ten years five years this is primary progressive they're just slowly slowly the disease is getting worse and worse and often actually disease actually appears later after forty years old and tend to have less visual or more axonal involvement compared to the secondary progressive whereby they have this relapsing remitting relapse remit relapse remit and that secondary progressive disease that eventually now start to get worse over the years and then they don't remit anymore see that they go up down up down and then they progressively gets worse and relapse every minute is they go up down up down up down up down and the first one is silent or benign now attacks often average about one a year so this patients can get at least one attack a year and there's really nothing that's been proven to cause this attacks nobody knows they message the weather it might be this might be heat it might be cold nobody really knows what really brings us this attacks now what is the prognosis of this disease it's highly highly variable some people have most people have a normal lifespan in most patients although the quality of life might be diminished right because of the above all the symptoms but many patients never really develop a debilitating disease to the point the idea just there they can't move anymore however about 1/3 of the patients we eventually go into disability to go to the permanent weakness or paraplegia they can't move any of their arms or their legs and that's usually one third of the patient that develop this now often patients have an increased risk of developing severe disability with if they have a lot of frequent attacks early up in the disease course and also onset that start at older age and progressive course and early cerebellar or parameter symptoms which means if the patient has a lot of frequent attacks at the beginning that is not a good prognosis and also causing them to diversity of severe disability and decided one third we talked about or unless somebody develops literally in their 60s over their 50s that is also can cause them to grow more disabled and if they have cerebellar which have perfect the cerebellum and they have a problem with the ataxia and also vision problems so how do we really make the diagnosis of multiple sclerosis what the diagnosis is actually a clinical diagnosis which means there's really no specific labs to really give out the diagnosis of multiple sclerosis so in the patients in a young patient in the 20 or 30 s that you simply that having this relapsing and remitting symptoms they come in complaining of all this neurologic signs and symptoms it's often very difficult because this have this patch here this numbness on my belly it doesn't really fit it doesn't really feel like they're not having a stroke or anything like that so often that's why it's always the clinical diagnosis and it's often difficult because these patients are having a lot of white matter involvement however a suspicion if you think a patient have multiple sclerosis you're going to order an MRI clinical diagnosis if you suspect it all right you haven't all this neurologic symptoms you can't really explain then you order huh magnetic resonance imaging this is very important or you can also do an LP which is a lumbar puncture to see what the CSF is MRI by far is the best and the most sensitive tests of choice to make the diagnosis on any patient that have multiple sclerosis and often what you're going to be able to see on Emma is a lot of demyelination off the cns that's why we order an MRI so often 90% of patients are ms I'm gonna have abnormal abnormality in the under MRI and there's CSF which we're gonna get from which is a cerebral spinal fluid is gonna show it's going to be also abnormal in fishing that have multiple sclerosis now when you do LP and you do a CSF analysis of often although there's really no lab specific test we are looking for in this case what you're gonna see our only go clonal bands of immunoglobulin G oligo clonal bands of I Gigi and that's what you're looking for inside the CSF and in ninety percent of the time ninety percent of MS patients you're gonna see a good over the colonic bands of immunoglobulins and on MRI you'll be able to see d miley nation also if you see evoked potentials can also suggest demolition certain areas when they do speed of nerve conduction within the brain so basically what they do they're testing how fast the nerve axons of the neurons inside brains are firing if the see evoked potentials evoked potentials that is basically telling yours that you have some newly d myelinated area inside remodeling the nerves inside the inside the brain alright so how do we treat these patients right I start from checking for evoked potential looking for demyelination using MRI and also using an oligo cloner band well the treatment often depends if when they have an attack if this fishes have an acute attack acute exacerbation like I say relapsing our relapsing episode you want to start them off steroids you want to give the high dose intravenous cortical steroids that's what you're gonna give the patient that has an acute attack also patients can also be given disease modifying therapy this is modifying therapy and this is actually we can use interferon interferon what kind of interferon do we often use we use the beta 1 interferon and the recombinant beta 1 B 1 a and beta 1 B decided to interferon agents we use and you can also use serum s acetate glad serum er acetate which is the drug of choice to help reduce R in the relapse rate of patients that have multiple sclerosis however when we give interference I have to let you know that interference actually can give you flu-like symptoms it's basically like giving you a drug that's gonna make give you a flu so this is just drugs are not benign at all although they are good in reducing relapse in the patients they have a lot of flu-like symptoms they have you know they have weakness in their arm they feel really really horrible when they take these medications but this is often the drug that's necessary to help this patient often interferon therapy should be started early in the course of the disease and this is because so because you want to prevent this patients for going to permanent disability all the drugs we can give are baclofen and baclofen is actually given for muscle spasms and also you can give carbamazepine or gabapentin or neurontin if they have neuropathic pain the drug of choice for trigeminal neuralgia is carbamazepine but anytime a patient comes to the hospital and they have neuropathic pain twitches nerve pain the best drug to give is also gabapentin gabapentin and this will help relieve their symptoms especially if they having a lot of symptoms remember there is no cure for multiple sclerosis there's only two primary goals you're going to want to do for this patient number one you want to prevent a relapse you don't want the disease to keep coming back and number two if they have an acute exacerbation of the disease you want to relieve that exacerbation often relapse of multiple sclerosis produce symptoms for longer than about 24 hours and they average about one a year but usually over time they start to decrease especially if you try to get them on treatment as soon as possible well that brings us to the end of multiple sclerosis how be able to understand the disease and it's entirely remember this is a demyelinating disease of the white matter inside the brain it can affect different tract parameters rubella Emma laughs right also we can affect the optic nerve at the back of the eye and the posterior columns patients often come in complaining of this nonspecific patterns of neurologic symptoms patches of sensory loss some random weakness or specificity in their hands visual problems you just wonder like okay there's no I can't really put a tract on where the disease is you know this doesn't make any sense you know it's not like somebody had a stroke in the house complete weakness in their arm or spasticity or anything like that and then you said okay you know your visual problems oh well I got this black spot in the center that's a central scotoma well you can't really pinpoint ever after girag disease because they're usually 22 30s so you don't expect them to out maybe an emboli and anything like that as blocking an artery in their brain so this makes no sense that's when you go ahead and order an MRI and the MRI will be able to highlight the areas of the brain that have the cortical demyelination part and then you want to do an LP to check for the oligo coronary bands of the immunoglobulin G which is often found inside the cerebral spinal fluid you can check for evoked potential to look for demyelination disease causing decrease firing of the action conduction system within the brain and then if they have an acute exacerbation which is usually happens in patients that have relapsing remitting you want to start them on steroids right away the drug of choice to treat other symptoms are the interferon beta one and the way I remember it is it's better to treat MS so it's better 1:8 and bitter 1b and go a tumor acetate baclofen for muscle spasm carbamazepine and gabapentin for neuropathic pain thank you very much for watching it's doctor additional from FTP lectures calm till I see you again have a great day bye bye

Channel: Dr. Adeleke Adesina, DO

Views: 32,143

Rating: 4.8662953 out of 5

Keywords: multiple sclerosis, MS, demyelinating disease, nervous system, peripheral nervous system, tingling, numbness, weakness, ftplectures, nclex, USMLE, COMLEX, internal medicine, neurology, nervous system disease

Id: JkDp7ldTqb0

Length: 49min 12sec (2952 seconds)

Published: Wed Aug 15 2012