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Adem Application Form Demand Assistance

good morning ok let's start I'm talking.on acute disseminated and stuff alone.myelitis or as we say commonly a.m..acute disseminated encephalomyelitis is.a mouthful so I'll keep it at a.m. it's.usually a mono phasic illness that.affects the brain and spinal cord.typically after of viral a febrile.illness it's also been described after.bacterial and parasitic infections as.well it's commonly in children but.adults encounter it from time to time.and there have been a lot of reports and.adults as well the pathogenesis is.thought to be multifocal inflammation.associated with demyelination related to.an autoimmune phenomenon on pathology we.see Perry venous invasion of lymphocytes.and monocytes associated with.demyelination so what causes a Dem well.in a review from Tannenbaum neurology.she found that the not 35% of the time.that nonspecific URI symptoms are.encountered prior to and prior to making.a diagnosis and we see here a 26% no no.preceding infections were available were.found in her series vaccination is is.1/3 and 12% we used to see this more.after vaccinations before.so the original disorder was named post.viral exam and cephalo mellitus.following a measles infection typically.1 to 2 weeks afterwards it always had a.very poor outcome and patient and.children usually died in some cases you.can refer to a them as post vaccine and.cephalo myelitis as well so the lesions.in agent predominantly affect the white.matter of both the brain and the spinal.cord and there are multiple lesions and.areas of demyelination are also seen and.described in the cerebral cortex.alamos hypothalamus and basal ganglia on.the deep gray matter on neuro.pathological examination limit there's a.limited extent of demyelination when you.just and that's a way that you can help.distinguish between a.m. and MS.however histological features of both.may certainly overlap so what how do.patients present to the hospital what.are their symptoms at the time they they.come into the emergency room there have.been a several there have been several.reviews but they've all been largely.retrospective and observational studies.all these reviews had good number of.patients that underwent who underwent a.detailed workup so let's review some of.some of these reviews I just quoted a.few few studies here and we can see the.top three or four diagnosis is headaches.and fever altered Mental Status.encephalopathy impaired consciousness.have also been described early as a.manifestation what else can we see well.these reviews have also mentioned.seizures visual impairment bilateral.optic neuritis and many children.presented with Polly's had a poly.symptomatic presentation that's more.than one symptoms at the time of.diagnosis so onset to peak deficit is.usually less than 24 hours but some.investigators have found that the peak.deficit can can be found up to 30 days.and recurrence has been reported by.several Arthur's authors and I'm going.to talk about this a little bit so.incidents of edom is 0.4 per hundred.thousand with a median age six point.five years there's a slight male.predominance and recovery is generally.good time to recovery from any new from.the neurological illnesses is deficits.is anywhere from a month to six months.so before we label a child with a dam we.have to be really vigilant.about other CNS pathologies such as.acute and antiphospholipid antibody.syndrome vasculitis from college and.vascular diseases neoplasia azure tumors.neuro sarcoidosis another inflammatory.condition of the CNS mitochondrial.encephalopathies dis myelinating.syndromes and and of course ms so.cerebral spinal fluid is definitely an.investigation that's done on anyone that.comes in with suspected a dem so we've.we can find a variety of CSF findings.including mild plio cytosis with the.lymphocytic predominance mild protein.elevation all ago kono bands have been.reported but they are not common so i.think the highest al ago Conal band rate.in a study was was about six in in a.very large case series and oftentimes.CSF can be normal so just because it's.normal it doesn't rule out the diagnosis.so MRI features are plenty as we as i've.listed the whole laundry list MRI is the.diagnostic imaging of choice and we see.here predominantly affects the white.matter deep gray like I mentioned before.the hypothalamus the thalamus basically.ganglion or both bilateral thalamic.involvement have been reported by.several authors and the cortex has also.been which is gray matter has also been.involved we can see vague enhancement.hemorrhage is rare but can be found the.corpus callosum is usually spared in ms.this is it's commonly involved.periventricular lesions are not common.in a.m. but but more are very common in.ms and new lesions are typically not.seen and follow-up imaging that's when a.child recovers and you get another MRI.done and new lesions should not be found.in a.m. and in and don't forget an.initial MRI may be.normal as well and it can affect the.spinal cord I didn't write the for.spinal cord features here so Tannenbaum.from neurology 2002 classified her.patients into four distinct groups.according to neuro imaging features.group Akins was the majority 62%.multifocal and these patients had.multifocal small white matter lesions of.demyelination x' large confluent tumor.like lesions were found in Group B and.she found symmetrical bilateral thalamic.involvement in Group C and there were.only two patients in her group that had.hemorrhagic lesions so you can see it's.a variety they can present with very.different neuroimaging features and here.this is the tumor like lesions that.people with Group B had this is from.Tannenbaum's.review so it looks pretty scary and so.you can see deep grey matter.deep grey nuclei involved here I circled.it for you and this sort of compares 8 m.to M s we can see in a dem the cortex.involved the deep gray matter.involvement and here in M s we see.periventricular lesions that are very.common and these are elliptical or ovoid.and perpendicular to the ventricle.that's pretty characteristic of an MS.brain so how do we treat these patients.IV therapy steroids methylprednisolone.is the treatment of choice 20 to 30.milligrams is what it's commonly used.but some authors have used 10 to 20.milligrams as well and this is followed.by a prolonged oral taper of prednisone.decks dexamethasone can also be.substituted if necessary IVIG has been.given for those who don't respond very.well to steroids and even plasmapheresis.in fulminant a demand those who require.ICU admission who have hemorrhagic.lesions these patients can be tried on.with plasmapheresis.so what's the outcome in these children.it's usually very good with complete or.near complete recovery found in ninety.percent not eighty nine seventy one and.eighty three percent from these various.studies just to name a few.some children are left with some.residual disabilities ICU admission and.ventilator support may be necessary and.death is not common but it can occur and.relapses can occur and of course it's.not commonly encountered so let's talk.about relapsing or recurrent am several.reports have have been described several.authors have found various number of.patients who have this relapsing form of.a.m. we have a few patients ourselves.that we follow with this condition so a.few questions come to mind is this ms.how do we treat it what is the long term.clinical outcome of these patients and.the answer is I'm not sure so how do we.define relapsing a damn it's two or more.separate acute episodes that differ in.clinical presentations and other.questions.found in the literature's is this.condition a separate clinical syndrome.or it's part of the MS spectrum another.term that describes relapsing am you'll.probably hear or you'll probably read in.the literature is multiphasic.disseminated encephalomyelitis MDM and.this is used by a few authors so let's.see how many people in in these studies.have actually relapse well we see four.we see eight 10% but the highest is.reported by an lar with 33% so far in.the literature so how do we treat these.relapses well the same as that for.monophasic.am IV steroids we may consider standard.immunomodulatory there.be such as the ABC our drugs used to.treat multiple sclerosis but we we don't.know what it does for this condition and.there's really no evidence available at.this time so how can we distinguish.relapsing a.m. from ms well we can look.at the first clinical the age of onset.of the first clinical symptom um usually.a.m. children are younger and symptoms.that presentation do they have a poly.symptomatic presentation headaches fever.that goes more along with a dam rather.than ms and possibly a CSF parameters.such as all ago clonal bands and that.would sort of give a give us a favor ms.and possibly MRI features acutely.imaging during convalescence during.recovery and patients with 8m we should.not see new new lesions family history.of ms can certainly help and more.sophisticated in neuro imaging.modalities have been have been reported.with magnetic resonance spectroscopy and.diffuse diffuser tensor imaging DTI is.actually been reported with a Dem and it.it evaluates white matter changes that.are not otherwise seen on conventional.MRI white matter abnormalities that are.not seen on conventional MRI and a ten.patients are supposed reported to have.normal white matter compared to those of.ms with this imaging modality so it may.hold someplace but these are but it's.still in the research stage okay in.summary ADM appears acutely it's usually.found in children less than 11 it's.typically monophasic but as i've stated.there it relapses have been reported.encephalopathy which is also altered.mental status fevers headaches are the.initial symptoms a presentation and a.lot of children it can affect oops sorry.it can affect both white matter and.the recovery is generally good and MRI.may normalize should have put may may.normalize during convalescence oops so I.have a case here very brief case of a.patient of tho we and some pediatric.neurologists are following I just.thought I would share it with all of you.this is an 11 year old Caucasian girl.with recurrent episodes a weakness.associated with headache and altered.mentation seizures were associated with.some of these relapses she began having.her initial symptom actually was at the.age of 6 and she has a family history of.lupus CSF was obtained initially and.subsequent visits to subsequent relapses.and all of Okolona bands IgG index were.negative.she was then started on Copaxone 2 two.years later after initial presentation.thinking maybe this will will help her.relapses but she continued to have them.she had been doing well in school up all.along after I'd seen her she we switched.her to rebus and then it was it's hardly.been in a year it's only been actually.seven months she respond we think she's.responded but it's time is really short.so this was her I think her second MRI.scan you can see how extensive these.lesions are there even periventricular.but look at a look at the white matter.it's it's huge so this was another.relapse and during another relapse you.can see extensive white matter.involvement here I don't have her recent.MRI scan because we have a different.system in our Hospital and I wasn't able.to cut and paste but then she just had a.few periventricular lesions so it was.not dramatic and most of those lesions.had resolved and so again we don't.really know how to treat these patients.but we're treating them as.multiple sclerosis and only time will.tell to see whether they respond to this.form of therapy or not thank you and.this concludes my presentation.

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How long do Adem symptoms last?

How and when will this pandemic end? We asked a virologist We may be approaching a saturation point in terms of coronavirus infections in some of the worst-hit countries. Eventually, the virus will run out of people to infect.But there are still many unknowns when it comes to this virus. We spoke to Belgian virologist Guido Vanham, the former head of virology at the Institute for Tropical Medicine in Antwerp, Belgium, and asked him: how will this pandemic end? And on which factors might that depend? More than one-third of the world's population is now in lockdown as the world battles the COVID Continue Reading

Can you die from Adem?

More than "just" one of the formerly obiquitous and very infectious childhood infections, it causes the infected person's body to have less immunity against other infectious diseases, up to three years after, so quite disturbing, see this 7 May 2015 paper by Michael Mina et al Vaccines. Long-term measles-induced immunomodulation increases overall childhood infectious disease mortality. From a discussion on Measles May Weaken Immune System for Up to 3 Years, Study Contends: MedlinePlusNew research suggests that children who survive a measles infection remain vulnerable to other potential Continue Reading

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