How to cure respiratory infections are severe

over the next several minutes i’m going to discuss very briefly some historicalaspects of guillain-barre syndrome. i will then focus on the clinical features of guillain-barreincluding some of the variance we see in clinical practice. i will talk a bit about the diagnosticapproach to the disorder including consideration of conditions in the differential diagnosisof the presentation. i’ll focus very briefly on the pathogenesis of guillain-barre, andthen spend the rest of the time talking a little bit about the treatment and some prognosticaspects of the disorder. i don’t have any conflicts of interest that are relevant tothis presentation. i would like to take this opportunity to thank dr. elizabeth raynor,my colleague, and dr. ted burns for sharing

some of their slides with me. in 1859 landry first described a case of distalsensory formications and ascending weakness after a prodromal illness with fever, malaiseand pain; and this patient progressed to paralysis over three weeks and died from respiratoryfailure. in addition, he also described four similar cases. sixty years later two frencharmy neurologists, guillain and barre, described an acute neuropathy in two soldiers and theclassic cerebral spinal fluid finding of albuminocytologic dissociation. strohl did the electrodiagnosticstudies in these soldiers, and these authors distinguished the illness from acute paralyticpoliomyelitis. the 1950s and 1960s really saw tremendousresearch into the pathophysiology of the disorder

along two paths. one, to delineate the electrophysiologicfeatures of the disorder and the other along the lines of pathogenesis and immunology.the 1980s and the 1990s were the decades of immunotherapy. guillain-barre syndrome is an acute monophasicimmune-mediated polyradiculoneuropathy with a mean age of onset of about 40 years thataffects slightly more males than females. it affects persons of all ages, races andnationalities. the worldwide incidence of guillain-barre has been reported to be anywherefrom 0.6 to 4 per 100,000 annually. children tend to be affected slightly less frequentlywhereas adults over the age of 50 years have a slightly greater incidence of the disorder.two-thirds of cases of guillain-barre syndrome

are associated with an antecedent infection. the typical clinical presentation of the diseaseis an acute generalized motor greater than senseory syndrome. the official name of thedisorder is “acute inflammation demyelinating polyneuropathy” which emphasizes the timecourse and the pathology of the disease. i will use the term gillain-barre syndrome inthis talk to encompass aidp and all its variance. the most common initial symptom of guillain-barreis paresthesia of the distal extremity, however at this stage, patients have little objectivesensory loss. severe radicular back pain or neuropathic pain affects most cases and iscommonly seen in the whole spectrum of guillain-barre and its variance.

diagnosis of guillain-barre, especially earlyon in children can be difficult and a high index of suspicion is necessary because childrenmay just present with pain, difficulty with walking or even just plain refusal to walk.within a few days, weakness ensues commonly in a symmetric ascending pattern. however,weakness can be somewhat asymmetric especially at the onset of the illness. most patients present initially with proximalas well as distal weakness in the lower extremities that subsequently spreads to the arms. thisis the presentation in approximately half the patients. a third of the patients presentwith both leg and arm weakness, and a few patients, approximately 10-12%, have onsetof weakness in the arms. facial nerve involvement

occurs in 70% of the cases and otopharyngealweakness or bulbar weakness with dysphagia in about 40%. rarely, approximately 5% ofpatients may develop ophthalmoplegia, ptosis, or both, and in this case the differentialdiagnosis of botulism or myasthenia gravis arises. hearing loss, papilledema and vocalchord paralysis are less common. a quarter to a third of the patients go on to developrespiratory failure requiring ventilatory assistance. autonomic dysfunction predominantly in theform of cardiovascular dysregulation is presented in most patients if carefully looked for,but the severity varies quite highly. most often, dysautonomia is in the form of sinustachycardia, but patients may also have bradycardia,

labile blood pressures with hyper and hypotension,or just plain orthostatic hypotension. they may develop cardiac arrhythmias. they maydevelop even neurogenic pulmonary edema and may report changes in sweating. a smallerpercentage of patients, approximately 5% may have dysautonomia that affects the bladderin the form of urinary retention or incontinence or the bowels in the form of constipation,ileus, gastric distention or even fecal incontinence. and in these patients, a differential diagnosisof a spinal cord disorder arises. this table is from the review from dr. alanropper in the “new england journal of medicine” in 1992 and if you look at the top columnor row, paresthesia are frequent initially in approximately 70% of patients, but thesepatients don’t often have sensory impairment.

at the peak of the illness however, both paresthesiaand sensory impairment are seen in the vast majority of patients. weakness involves the legs more than the armsinitially, but at the peak of the illness involves both the arms and the legs in mostpatients. the legs are affected more than the arms in over half of the patients, andapproximately a third of the patients have equal weakness in the legs and the arms. some patients progress rapidly to become ventilator-dependentwithin hours or days, whereas others have mild progression for several weeks and neverlose ambulation. occasional patients may have a stuttering or even a stepwise progression.weakness may range from mild to severe flaccid

quadriplegia; and about a third of the patientsnever lose ambulation. the nadir of the weakness as you see in the picture here is reachedby two weeks in anywhere from 50 to 80% of patients depending on the series. these patientsthen enter a plateau phase, again the duration of the plateau phase varies. the median wasfound to be approximately one week in the large study published in “brain” in 2014that evaluated almost over 500 patients with guillain-barre syndrome. following the plateauphase, patients gradually start to recover there have been diagnostic criteria establishedfor guillain-barre syndrome. the asbury criteria was the initial criteria. more recently wehave the brighton criteria, which provides a level of diagnostic certainty from leveli-iv. however, overall, the features that

are required for the diagnosis include progressiveweakness in more than one extremity associated with areflexia or at least hyporeflexia. some features that strongly support the diagnosisinclude the fact that progressional symptoms occurs for a period of less than four weeks.there’s relative symmetry of motor weakness, although as i mentioned earlier, it may beasymmetric at the onset. sensory symptoms and signs tend to be mild, but we do needto bear in mind the fact that there is a sensory variant of guillain-barre syndrome and i willtalk about that. bilateral facial weakness and autonomic dysfunction when present supportthe diagnosis and the typical cerebrospinal feature of high concentration of protein withthe lack of clear cytosis and typical electrodiagnostic

features, often acquired demyelinating syndrome,further support the diagnosis. having spoken about the typical presentation,let’s focus a little bit on some of the variants that we see in clinical practice.the first variance that was described was miller fisher syndrome and many of you arefamiliar with this presentation of ophthalmoplegia, ataxia, and areflexia without weakness. mostpatients present with at least two of these features and they do have an elevated cerebrospinalfluid protein, and that as many of you are aware, they have the characteristic autoantibodyto ganglioside gq1b. in the western hemisphere, miller fisher syndromeaccounts for approximately 5 to 10% of cases but tends to be most frequent in eastern asia,accounting for up to 25% of cases in japan.

some of these patients may actually progresson to just develop the classic ai dp picture. bickerstaff’s brainstem encephalitis isa variant of miller fisher syndrome and is characterized by alteration in consciousnessthat may progress even on to coma. these patients have paradoxic hyperreflexia rather than areflexia.after initial descriptions of acute inflammatory demyelinating neuropathy, we recognized thatthere were some patients who had axonal features and the acute motor axonal neuropathy variantwas reported in 1993 from northern china. soon after that, acute motor and sensory axonalneuropathy was reported. these cases have also been described from other countries includinghere in the united states. the pharyngeal-cervical brachial variant presentswith ptosis, ophthalmoplegia, bifacial weakness,

pharyngeal or bulbar weakness, neck flexorweakness spreading to the upper extremities. these patients have spared sensation and usuallydon’t have weakness in the lower extremities. and as you can imagine, this really does bringup the differential diagnosis of myasthenia gravis or botulism. the paraparetic variant presents with backpain, bilateral leg weakness, numbness and areflexia that can mimic acute cord lesion.local or restricted variants such as bifacial weakness or bilateral sixth nerve palsieswith paresthesia have also been described. many of us who take care of these patientswill see either a pure sensory ataxic variance or acute pandysautonomia often associatedwith sensory features.

two-thirds of patients report symptoms ofrespiratory or a gastrointestinal tract infection before the onset of the disease and in abouthalf these patients a specific type of infection can be identified. respiratory infectionsare more frequent than gi infections. also, gi infections the vast majority are due tocampylobacter jejuni. mycoplasma is also a bacterial infection that has been implicated.of the viral infections cytomegalovirus is the most common usually associated with therespiratory illness as an antecedent. epstein-barr virus can also be associated. we do see guillain-barresyndrome with associated hiv, usually a seroconversion or an early disease, hepatitis c and of coursenow, zika. a few patients develop guillain-barre syndromeshortly after receiving a vaccine and despite

the fact that these are rare, obviously suchevents cause considerable public concern. even the vaccination campaign against influenzah1n1 in 1976 in the united states approximately 1 in 100,000 persons vaccinated developedguillain-barre syndrome. however, in the 2009 season the incidence was 1 per million thatwas felt to be no different than after any seasonal flu vaccine. a few patients had reportedantecedents of pregnancy, surgery or epidural anesthesia. there are some clinical features that shouldraise red flags to the diagnosis of guillain-barre syndrome. patients who present with severerespiratory involvement with limited limb weakness at the onset usually do not haveguillain-barre syndrome. similarly, severe

sensory signs with limited weakness at onsetis a red flag, although again you have to bear in mind that we may be just dealing witha sensory variant that i alluded to earlier. the bladder and bowel dysfunction in guillain-barrefollows a very specific pattern that one has to be aware of. usually, when patients developbladder and bowel dysfunction they do so at the height of their illness when they havemaximum weakness and that is transient, and usually recovers before limb weakness startsrecovering. so if you see a patient who has severe bladder or bowel dysfunction at theonset of the illness when weakness is not prominent, or if they have persistent bladderor bowel dysfunction during the illness that should raise a red flag to the diagnosis ofguillain-barre.

fever at the onset of illness is not usualbecause they’ve usually gotten over the antecedent infection sorry, and often timesat least when i trained in india and we saw a lot of paralytic poliomyelitis was childrenwho developed a febrile illness and along with the fever developed asymmetric weaknesswith extremely exquisitely painful limbs, usually have paralytic polio and not guillain-barresyndrome. other infections may also be at play here. obviously, a sharp sensory levelshould bring up the diagnosis of myelopathy. and if you have more than 50 lymphocytes percubic millimeter in the cerebrospinal fluid or if there are polymorphonuclear lymphocytesin the cerebrospinal fluid, both of these should bring up other differential diagnosis.

what is the diagnostic evaluation in thesepatients? a careful history and neurological examination is important followed by laboratorytesting, magnetic resonance imaging of the brain or the spine as appropriate, followedby electrodiagnostic studies and lumbar puncture. and i state this in no particular order. the mental side of the examination in thesepatients is usually normal except for the few patients who have brainstem encephalitis.the cranial nerve examination typically reveals normal pupils and that’s an important factorwhen you see patients with a pharyngeal-cervical-brachial variant and you consider a diagnosis of botulism,because botulism often affects the pupils because of dysautonomia. you may see ptosisand ophthalmoparesis, bifacial weakness is

common and of course, bulbar weakness maybe seen in about 40% as i mentioned. the motor examination reveals both proximaland distal weakness, which is largely symmetric and legs are more involved than arms in mostpatients. the brain review that i mentioned earlier reported about 8% of patients witha paraparetic presentation. sensory involvement is in the form of large fiber sensory lossand therefore involves vibration and position sense. the ankle jerks are usually large first.later, most patients develop diffuse areflexia or at least hyperreflexia. in the same series of the brain, approximately10 percent had normal reflexes, despite having weakness in their arms; and 2% despite havingweak legs. and in some of these patients normal

reflexes persisted in the arms later on inthe disease course as well. a small proportion of patients with guillain-barr㩠syndrome,especially the acute motor axonal neuropathy variant, may have preserved or even exaggerateddeep tendon reflexes, as also the patients with bickerstaff’s encephalitis. howeverfor most parts, the presence of exaggerated reflexes should prompt you into consideringacute myelopathies in the differences in diagnosis routine laboratory tests are usually normal.some patients may have mild elevation of serum creatine-kinase, mildly elevated liver enzymesmay be seen. consideration should be given to testing for lyme antibody titers, heavy-metalscreens, toxicology screen, urine porphyrin testing in the relevant clinical context.consideration to hiv testing, again, if there

are risk factors for hiv. please bear in mindthat because the disorder occurs at fetal conversion or early on, the appropriate testto get is a pcr for a viral load and not the antibody testing because they may be antibody-negative.campylobacter jejuni antibodies really offer only prognostic information, and we will talkabout that later. there was a lot of literature about anti-gangliosideantibodies in the ‘80s, maybe the ‘70s and ‘80s and the ‘90s probably. however,usually they do not change management, and they are not ordered in the clinical setting.the exception to this perhaps may be in the second where miller fisher or bickerstaff’sbrainstem encephalitis is suspected when we tend to order gq1b antibodies because of thehigh sensitivity and specificity. but the

fact remains that for the most part, the resultof these antibody testing is not available before we start treatments in these patients cerebrospinal fluid protein elevation withoutclear cytosis, the typical albuminocytologic dissociation, is the hallmark of guillain-barrã©syndrome. however when performed in the first 48 hours, 85% of patients may have normalprotein, about two-thirds had elevated protein in the first week of the illness, and morethan 90 percent do have this pattern in fully developed illness. pleocytosis is unusual. as i mentioned earlier,if you have more than 50 cells per cubic millimeter, several differential diagnoses arise, includingearly hiv infection, lyme disease, leptomeningeal

carcinomatosis, cmv polyradiculitis, sarcoidosis,and other inflammatory or infectious conditions. the absence of albuminocytologic dissociationin the first week does not exclude guillain-barr㩠syndrome, and that’s important to remember. these two boxes are from the same paper anddrain. if you notice in the upper box, normal cell counts of less than five per cubic millimeterwere present in the vast majority of these 500-odd patients. more than 50 cells werenot seen in any of these patients. the lower box looks at protein elevation in the cerebrospinalfluid as a factor of the time between weakness and the lumbar puncture. in the first coupleof days only 50 percent of patients have elevated proteins. by the end of the first week, two-thirdsor more have elevated proteins, but that still

leaves us with the one-third who don’t havethe elevated protein. that’s important to remember. the goals of electrodiagnostic testing inguillain-barr㩠syndrome are to localize abnormalities to the peripheral nerve and to demonstrateevidence of a acquired demyelination. early electrodiagnostic findings may be subtle andrepeat studies may be required if the diagnosis is in doubt. the focus of the study is onnerve conduction testing, rather than needle emg, but both of these are complementary again in that same series from brain 2014,in the first week of illness, approximately 48% of patients had demyelinating featureson nerve conduction studies but 41% had equivocal

nerve conduction studies. i will spend a few minutes talking about thedifferential diagnosis of the disorder. if you think about it, guillain-barr㩠syndromepresents as an acute low motor neuron disorder with weakness and areflexia. so let’s talkabout all of the low motor neuron syndromes, starting from the anterior horn cells andgoing down in the neuroanatomic fashion. acute myelopathy, as we mentioned earlier,are in the differential diagnosis – especially if you have suspicion for a spinal cord level.they may be compressive or non-compressive. and the problem is that in the acute phase,you may have spinal shock and therefore limbs are flaccid, and reflexes are absent and thesetone and reflexes don’t help you distinguish

from an acute myelopathy. in addition to acute myelopathy, focal disordersof the anterior horn cells as part of paralytic poliomyelitis or west nile virus infectionmay cause a low motor neuron type of paralytic presentation. many of these presentationsare thick with evidence for meningitis, fever, et cetera. coming down to the peripheral nerve, criticalillness neuropathy can present with a similar picture, but it’s diagnosed by the companyit keeps. so patients are sick, they are in the icu, they have sepsis, they have multi-organfailure, et cetera. lymphoma or leptomeningeal carcinomatous meningitis often times are associatedwith sensory involvement as well. toxic neuropathy,

solvents, heavy metals – we have thallium.you have arsenic. most of these patients have g.i. symptoms. they have skin manifestations.thallium causes alopecia and [inaudible] manifestations. a brief mention of marine toxins – thesepatients often present with severe paresthesia followed by weakness very rapidly. they canalso have dysautonomia. here i’m talking about tetrodotoxin, which is due to pufferfishingestion or saxitoxin or ciguatoxin. the history is really key here. porphyrias – youknow the presentation with the typical abdominal pain, the photosensitivity, urinary findings,et cetera. vasculitic neuropathy is associated with other features of systemic involvement. we spoke about myasthenia gravis and botulismin the neuromuscular junction. hypermagnesemia

is an infrequent cause of neuromuscular junctionblockage. in children tick paralysis can begin two to four days after the tick bite. it reverseswithin 24 hours after tick removal, and the process here is a motor nerve terminal channelinhibition. coming down to muscle, there are idiopathicinflammatory myopathies that can present quite rapidly sometimes. rarely, but you do seethem. rhabdomyolysis, critical illness myopathy – again, distinguished by the company itkeeps. periodic paralysis or secondary hypokalemia with paralysis, as well as hypophosphatemia. the bottom line however is that early guillain-barrã©syndrome is often the clinical diagnosis. ancillary investigations such as cerebrospinalfluid analysis and electrodiagnostic study

are useful to exclude an alternative diagnosisbut may not help to confirm early guillain-barr㩠syndrome. however, it’s important to diagnosethese patients early because early treatment improves outcome. i’m going to be very brief regarding pathogenesisin the interest of time. it’s presumed autoimmune, but we don’t know exactly what happens.a trivial infection triggers a humoral response and these antibodies cross-react with gangliosidesin the phenomenon of molecular mimicry is. there is complement activation, lymphocytecell infiltration of proximal nerves and nerve roots, and macrophage-mediated myelin strippingcausing segmented demyelination. the pathology of acute motor axonal neuropathy seems tobe slightly different, but i’m not going

to focus on this in the interest of time. what are the clinical pathological correlates?demyelination with conduction failure among motor nerve fibers is what leads to clinicalweakness. demyelination in large diameter sensory fibers leads to distal loss of vibrationand position sense. inflammation of peripheral nerve groups lead to pain, and inflammationof the autonomic ganglia causes dysautonomia. how do we manage these patients? supportivecare and immunotherapy are the two mainstays of their care. most patients with guillain-barrã©syndrome are admitted to the neurologic intensive care unit, or at least to an intermediarycare unit to reduce mortality and morbidity. we need to manage them very carefully andmonitor for respiratory failure, dysautonomia.

nosocomial infection is frequent, usuallypneumonia or urinary tract infections, and one needs to be vigilant to these infectionsand treat them aggressively. deep venous thrombosis and resulting thromboembolism are problemsin these patients who are often immobile and need prophylaxis with compression stockingsand anticoagulants. nutritional support, including nasogastric tube support or even percutaneousendoscopy gastronomy if bulbar paralysis lasts for a significant period is important. siadhcan be associated with guillain-barr㩠syndrome, and needs to be recognized and managed. ifneuropathic pain does not respond to non-[inaudible] agents, other agents – such as gabapentin,pregabalin, carbamazepine, oxcarbazepine, tramadol, et cetera – may need to be used.passive range of movement to prevent contractures,

prevention of decubitus ulcers and preventionof corneal ulcers in patients who have bifacial weakness is important. communication and emotionalsupport cannot be understated because even in patients who are not on the ventilator,this is scary. they get weak very acutely and unable to move. one needs to be able totalk to them about the prognosis, explain to them that they are going to get betterfor the most part. it’s key in patients who are on the ventilator because they’reoften completely conscious. clinical clues to impending respiratory failureinclude weakness of neck flexor muscles. you have them count after they take a deep inspiration,count as fast as possible. that’s called a single breath count. if it’s less than20 or 30 or if they have a poor cough at bedside,

these are signs that they have impending respiratoryfailure. they may also have tachypnea and paradoxical respiration. tachycardia and diaphoresismay also imply respiratory failure, although it may also imply just plain dysautonomia.the monitoring of these patients at the bedside is often performed by forced vital capacitymeasures or measures of maximal inspiratory pressure or maximal expiratory pressure. some of you may be aware of the data fromthe mayo clinic in 2001 that suggested the 20/30/40 rule for intubation and ventilation.if we see less than 20 mls per kilogram, mip less than minus 30 centimeters of water ormep less than 40. the problem with monitoring these is that it’s not easy for patientsto give you adequate effort, and there may

be variation between trials. you have to interpretthese in the clinical context. if the patient looks stable and the numbers look bad, thenyou have to really worry that the numbers may not be reliable. the mip and mep especiallymay be difficult in the presence of bifacial weakness because patients can’t hold onto the tube and give a good feel and blow hard. another reason to intubate these patientsprophylactically is an ineffective cough or an inability to handle secretions i call this the respiratory pyramid. thisis again from the ropper review in nejm. i really like this. the middle of the pyramidshows the vital capacity going from normal all the way down to five mls per kilogram.on the right side, you see the accompanying

respiratory pathophysiology, on the left yousee recommended ventilator management. at about 30 mls per kilogram, poor cough andsecretions start accumulating. just physical therapy is recommended. at about 20, the sighiscompromised, and atelectasis and hypoxia begin. intensive spirometry and deep breathing isnecessary. at about 15 is when patients are usually intubated dysautonomia can cause sudden changes in heartrate and blood pressure or arrhythmia, as i mentioned. it’s important when managingautonomic instability to be extremely conservative and avoid aggressively treating blood pressurefluctuation because patients tend to be very sensitive to medication. if you over treatthe highs, this may exacerbate the lows. for

instance, if you over treat tachycardia orhypertension, it may then result in patients with prolonged hypertension or bradycardia.it’s often best to avoid treating the fluctuations if at all possible. if treatment is necessary,the treatments are usually short acting medications rather than long-acting medications. one otherthing that’s important to bear in mind is to treat aggravating factors. pain can aggravatehypertension or of course tachycardia. hypovolemia can aggravate hypertension, and needs to betreated. the mainstays of immunotherapy – plasmaexchange and intravenous immunoglobulin. plasma exchange was the first treatment proven tobe effective in these patients in two large trials, the north american trial and the frenchtrial. in the interest of time, i will not

go through all the details on this slide butsuffice to say that in both studies plasma exchange performed within two weeks from symptomonset consistently demonstrated a statistically significant reduction in time to weaning fromthe ventilator by 13 to 14 days and in time to walk unaided by 32 to 41 days. in addition,the french cooperative study also demonstrated that the patients who required ventilatoryassistance after entry into the trial were significantly less in the plasma exchangegroup. intravenous immunoglobulin was first demonstratedto be efficacious in guillain-barrã© syndrome by the dutch guillain-barrã© study group twodecades ago. in this study, they compared ivig and plasma exchange. ivig was found tobe actually better than plasma exchange. this

then brought up the question – is it reallytrue that ivig may be better than plasma exchange? however, this slide shows you the north americantrial plasma exchange results and the dutch trial plasma exchange results. you will noticethat the group that received plasma exchange in the dutch trial really did not do as wellas the group that received plasma exchange in the north american trial. it says thatgroup imbalances probably account for this difference between ivig and plasma exchangein the dutch trial. in a subsequent large trial, the plasma exchange sandoglobulin guillain-barrã©trial conclusively showed that there is no real difference between plasma exchange andiv immunoglobulin. i will show you that in a couple of slides.

how do you give intravenous immunoglobulin?the dose is two grams per kilogram. whether to give it over the two days – that’sone gram per kilogram per day; or the same dose over five days, 0.4 grams per kilogramper day for five days – has really not been fully evaluated. there’s some data in childrenthat children who receive the shorter course had more treatment -related fluctuations thanchildren who received the longer course. what do we do with patients in whom we’vetreated them with either plasma exchange or ivig and it’s been 10 to 14 days, and theyare still significantly weak and not getting better? do we then treat them with the othermedication or other modality? if we give them ivig, it doesn’t make sense to give themplasma exchange after that because we are

just going to take away the ivig that we gavethem. if we give them plasma exchange, should we then give them ivig? the study that i mentioned– the plasma exchange and sandoglobulin guillain-barrã© study – looked at this.they randomize patients to three groups – plasma exchange alone, ivig alone, or plasma exchangefollowed by ivig – and conclusively demonstrated that there was really no difference betweengroups, meaning the plasma exchange and ivig were indeed equally efficacious; and plasmaexchange followed by ivig was not indicated. the american academy of neurology practiceguidelines for immunotherapy systematically evaluated all of these studies. the recommendationswere that treatment with plasma exchange or intravenous immunoglobulin hastens recoveryfrom guillain-barrã©. both of them are equally

effective, but plasma exchange may carry agreater risk of side effects and may perhaps be more difficult to administer. i think that’sreally what influences the choice of treatment in the clinical setting. combining the twotreatments is not recommended. i did not really discuss steroids for lack of time, but thisreview and subsequent reviews – including a cochrane interview – also found that steroidsare not beneficial in guillain-barr㩠syndrome. very quickly, plasma exchange requires a largedouble lumen catheter, usually through a central line – although there are centers that canactually do this with a prophylaxis. potential complications include blood pressure instabilityor hypertension. this can be a real problem in patients with severe dysautonomia. infection,pneumothorax, thrombocytopenia or anemia,

prolonged clotting parameters, hypocalcemia,or citrate toxicity are other problems. we usually monitor labs in these patients everyday. if clotting parameters are not optimal, we tend to hold plasma exchange. complications of ivig – infusion reactionsare not infrequent. they are usually managed with pre-medication and also with medicationduring the course of the infusion. the medications include acetaminophen, diphenhydramine, oreven intravenous nasal prednisolone if necessary. infusion reactions are also related to thespeed or the rate of the infusion. it’s important to start the rate slowly and escalategradually. when patients develop reaction, oftentimes dropping the rate helps with thesereactions.

acute renal failure is a rare but seriouscomplication seen in diabetics especially with underlying renal impairment related tothe use of sucrose as a diluent in the ivig. neutropenia and even thrombocytopenia mayoccur. heart failure as a factor of fluid overload may also be an issue. because ofthe hyper viscosity of the molecule, it is a big molecule. in patients who already haveunderlined risk factors of thromboembolism, thromboembolic complications have been described,albeit rarely. iga deficiency is extremely rare in the general population. patients whoreceive ivig can also have a delayed skin reaction with desquamation of the skin. i would like to mention briefly treatment-relatedfluctuations because i often get a call from

my colleagues about this in the clinical setting.approximately 10 percent of patients treated with ivig or plasma exchange deteriorate atleast one grade after initial improvement of stabilization. so they stop progressing,or they even get better but then they deteriorate. this is supposed to be due to a prolongedimmune attack on the nerves. the bottom line – again, not going into great detail. thebottom line is they usually improve after retreatment with the same modality they received.so if they received plasma exchange, a few more exchanges. or if they received ivig,retreatment with ivig – two grams per kilogram for another five days. when they have treatment -related fluctuations,it’s important to consider acute-onset cidp.

cidp is a chronic inflammatory demyelinatingpolyneuropathy and acquired polyneuropathy that can sometimes present very acutely. acutecidp should be considered when patients who are initially diagnosed with guillain-barrã©syndrome had three or more periods of clinical deterioration, or if their deterioration occurseight or more weeks after the disease onset. clinical clues for this is also the fact thatmany of these patients tend to have less severe weakness and maintain the ability to ambulateindependently at the worst of their weakness. they usually don’t have cranial nerve dysfunction.this differentiation is important because treatments are different. there is no real data regarding immunotherapyof variance. the bottom line is you treat

variance similar to treatment of aidp. similarlyin children, the treatments remain similar. prognosis mortality – approximately 5% upto 11% in some series. it’s important to remember that the mean time to complete recoveryis almost 7 months in 80% of cases. most improvement happens within the first year after onset,but can continue after this period, and it’s important to explain this to patients. about65% have minor residual deficits, and 10 to 15 per cent with significant residual deficitsin the form of weakness, fatigue, or pain. some prognostic indicators include older ageat onset of the disease, rapid progression before presentation, ventilator dependency,and preceding infection with cytomegalovirus or campylobacter jejuni.

patients with acute motor axonal neuropathyhave a more delayed recovery usually, but there are some patients who recover fairlyquickly because of the underlying pathophysiology. so it’s important to bear in mind that adiagnosis of acute motor axonal neuropathy does not necessarily mean bad prognosis. there is a very nice online prognostic toolthat is very useful in the clinical setting. this is from the international gps outcomestudy group. there are two of these scores. the egris score is the erasmus gbs respiratoryinsufficiency score. it predicts the probability of respiratory insufficiency within the firstweek of admission. the outcome score on the other hand predicts the probability of walkingindependently at two weeks after hospital

admission. the website is here in red andwhen you go into the website, this is what it looks like. it asks you to agree with theterms of use. you start the tool. it asks you what tool you would like to use. so whatdo you want to predict? do you want to predict risk of respiratory failure in the first weekor inability to walk six months after admission? you pick what you want. you put in your patientdata, and it will give you the score and also the risk in terms of percentage of eitherrespiratory failure or being unable to walk six months after admission.

How to cure respiratory infection that often recurs

it's february 29th. happy leap day to you.i'm julie moran. and i'm olga villaverde. do you actually knowanyone who was born in a leap year? no.i know. neither do i. did you know that 0.7% of the world's populationwas born on a leap day? well, i didn't know the exact figure, buti do know leap days only come once every four years. so, to have a leap year birthday isobviously very rare indeed. so true. and it's so appropriate that on thisday rare leap day, it's also world rare disease day.so appropriate here. as you know, we here at the balancing act are dedicated to rarediseases, and that's why we have our ongoing

rare disease series called behind the mystery.it's our way of keeping you informed and bringing you some of the most incredible stories ofcourage and medical advances. we're wearing and holding our denim ribbons in support,right here. yes. and matter of fact, coming up later thismonth you're going to meet a beautiful little girl who became that proverbial one in a millionwhen she was diagnosed with one of the rarest diseases in existence.and by one in a million, you literarily mean it. it only occurs one in every million births,right? exactly. these diseases are known to so fewpeople worldwide. so today we are thrilled to raise awareness for all rare disease patientseverywhere.

stay with us. the balancing act starts rightnow. (music).up first, we're bringing back one of the most touching stories. imagine you watch your ownmother pass away tragically of a rare genetic disease before she even reaches the age 50.that is so sad. but imagine having to then watch and wait looking for the same symptomsof the same deadly disease in yourself. it's just one of the devastating circumstancesfaced by today's rare disease patients including our first guest.he's young. he's talented. and as you're about to see, he's passionate about using his ownfamily's rare disease tragedy for a greater good. here's balancing act correspondent,chris cox.

dylan duncan is a songwriter and musician.he's also one of 50,000 patients impacted by transthyretin-mediated amyloidosis, orattr. i went in for my genetic testing at the ageof 26. so, i found out the had the gene for the disease, and a year later i got a fatpad biopsy, which was then used to determine whether or not symptoms had started.dylan duncan has been john berk's patient for nearly eight years. they know each otherwell. we met first in 2007, and at the time he wasi think 27-years-old. he had watched his mother become ill and undergo a liver transplant,and subsequently die. attr is a hereditary disease that culminatesin injury to nerves in particular and secondarily

to heart.dylan was 27 when he was diagnosed. but for him, it came as no surprise.how old was your mother when she was actually diagnosed?i want to say 37, 38. i know she was sick for about five years, and she passed awaywhen she was 45. the abnormal gene is passed from a parentto the patient, and it's approximately a 50/50 proposition every time an affected parenthas the child. people will typically develop some burning,tingling, or numbness initially of their toes, and there is evolution up the leg until theyreach approximately knee involvement. at which point, their fingertips and hands become involved.there can also be remarkable disfunction of

the gi tract so that diarrhea or profoundconstipation can be problematic. first symptoms that i was experiencing theamyloidosis were the carpel tunnel, which is what they say one in four patients experience.but it was very strange. like i would feel complete numbness in my entire arm, and i'dhave to hang my arm over the bed just to get the feeling back. and that happened around26, 27. that's why i went in to get tested. things were starting to develop when my gastrointestinalissues and numbness more in my calves i was experiencing, and i've heard that a lot ofthe numbness will happen kind of starting in the feet and going upwards.while currently there are no drugs specifically approved for attr in the united states, thereare limited treatment options.

there are clinical trials ongoing right nowthat are focused on not simply stabilizing the abnormal protein but eliminating it completely.new treatment options currently under development may give attr patients and their familieshope for the future. we imagine a world where patients with attrare living full, healthy, high-quality lives. but it's important for patients to get involved.diagnosis is critical, so we ask patients to get heavily involved in their diagnosisand bring others if they, in fact, do get diagnosed with ttr mediated amyloidosis inbecause it is a dominant autosomal inherited disease.dylan duncan continues to perform his favorite hobbies such as painting. he also enjoys hangingwith his group of supporter friends, and of

course, he continues to play his guitar.there's one particular song that you wrote called hello amy. tell us about that song.amy is short for amyloidosis, and so what i did was i actually wanted to just personifyit and make it almost sound like it's a girl that you want out of your life, like an ex-girlfriendor something like that. you know? (singing)."hello amy. i didn't expect you here this soon. you're not due for quite a while."there are moments when i get really really scared, especially since symptoms are startingto kind of show themselves. it's hard not to think negatively sometimes just seeingwhat happened with our mother. but absolutely, there are so many new advances that weren'thappening around the time that my mom was,

or if they were, at least they weren't beingso widely explored. it's very encouraging and very hopeful.for more information on a free third-party screening program, go to ttrscreen.com orcall toll free 1-855-338-3721. (music).(music). like many young boys his age, 7-year-old jacksondunn-kraus has many interests and he loves hanging out with his twin sister. his parentssay he is a funny kid and likes to laugh. this, despite his medical condition, jacksonhas a rare, serious, and progressive genetic disorder that affects mostly boys. jacksonhas hunter syndrome, the topic of today's discussion on this rare disease day. our gueststhis morning, dr. barbara burton, a professor

of pediatrics at northwestern university,and dr. david molter, a professor of otolaryngology washington university school of medicine atst. louis. and we're going to meet jackson and his mother a little bit later in the show.good morning to both of you. good morning.thank you so much for being here. dr. burton, let me start with you and let's talk abouthunter syndrome. what exactly is it? hunter syndrome, also referred to as mucopolysaccharidosisor mps type 2 is a rare genetic disorder that affects males almost exclusively. it is estimatedto occur in about 1 in every 162,000 births. it's a serious and progressive condition forwhich we currently have no cure. and let's talk about, doctor, the physicalsymptoms that maybe a parent notices. when

do they become noticeable? what happens?well, typically a baby with hunter syndrome appears healthy at birth, but then at somepoint in the early years of life symptoms begin to develop in multiple organ systems.there can be recurrent respiratory and ear infections. we see changes in the facial featurescalled coarsening resulting in thick lips, broad nose, large tongue. we also see an enlargedabdomen from enlargement of the liver and spleen. there can be chronic or recurrentdiarrhea. hernias are quite common, and we see progressive symptoms in the skeleton andin the joints, particularly progressive stiffness of the joints.dr. molter, i want to bring you into the conversation, and i do want our viewers to know that youare a otolaryngologist, which is also known

as an ent specialist: ears, nose, throat.do you see any common threads between let's say a baby that's born healthy and then obviouslythen symptoms occur? common threads between both?certainly. well as an ear nose and throat specialist, we see things ear, nose, throat,and dental. and so often this begins with a course of recurring ear infections whichmay lead to placement of tubes, sinus infections, upper respiratory infections, and changesin the facial features. we may see coarsening of the tongue, enlargements of the tonsilsor adenoids, and may see some changes in the teeth which are often described as being peg-like.well, these symptoms by themselves are certainly not a red flag and are common experienceswith childhood. it's when they're associated

with other findings such as a hernia or thecoarsening of the facial features that should begin to raise a red flag for hunter's.dr. burton? exactly. i think when you see multiple medicalissues in the same child, that's when you want to see if there's a common thread ordiagnosis that would explain all of those. and so a pediatrician or an ent doctor mightget suspicious, and then a specialist like myself, a geneticists, can recognize the combination,order the appropriate diagnostic tests, and make a diagnosis.and dr. molter, for parents out there who may be experiencing this, they don't knowwhat's going on, they're going from doctor to doctor. it can be extremely frustrating.it is their child. what would you say in terms

of maybe educating them and helping them sothey can find the answers they need? well, it certainly is challenging. it's whenyou find that you're reaching challenges outside of the norm that referral to a geneticistwould be appropriate. alright, dr. molter, i know you have to getgoing. dr. burton, you're going to stick around. thank you so much, dr.molter, for being herethis morning. because when we come back, we're going to meet jackson and his mother, a veryspecial boy. and we're going to share their story with you. so stay with us.(music). (music).welcome back, everyone. we've been discussing a serious progressive genetic disorder calledhunter syndrome. and joining us now are carrie

dunn and her 7-year-old son, jackson dunn-krauswho has this disorder. good morning to both of you.good morning. thank you for having us. oh, thanks for being here. doctor, beforei speak to this lovely young man, let's talk about hunter syndrome. now, we talked abouttwo forms: mild and severe. which one does jackson have?jackson has a mild or perhaps intermediate form of the disorder where there's littleor no involvement of the brain. many patients with hunter syndrome have the severe formwhere the brain is more extensively involved and we see more severe developmental delayor loss of developmental skills. now jackson, i hear you're seven. when areyou going to be 8-years-old?

on april.what day in april? umm…april 28th? oh!april 28th. oh, special day. and what grade are you in?2nd grade. and somebody told me this morning that youlove school? what's your favorite subject? science and recess.science and recess. perfect. we study for a little while and then we go play. i lovethat answer. definitely.carrie, let's talk about jackson. tell me what happened. obviously from what i've beenlearning here, he was born and everything

seemed healthy at the beginning.that's a great question. when jackson was first coming to us, we realized that we werehaving twins. so i was followed by a high-risk pregnancy physician. when he was born, hespent some time right away in the nicu because of a collapsed lung. so, he was having somedistress, pulmonary issues, and he spent some there and then they handed us our healthybaby and said, "go enjoy the twins." and sydney was growing a little bit faster and gainingher milestones a little bit earlier. jackson was showing some signs early on that distressedus a little bit in that he had a large distended belly. his skin was extremely taut. he wascrawling, what we'd like to call, commando crawl where his sister started walking.and still you didn't know?

we didn't know. but we did seek the adviceof numerous physicians and we started therapies early on. jackson started with occupationaltherapy, developmental therapy, speech therapy, sensory, feeding therapy, a little bit ofeverything, and this was all before he was three.and when was he finally diagnosed? right after his third birthday. we had gottena recommendation to see a geneticist and as we went into the geneticist's appointment,she discovered a hernia right away. so, the red flag was he has a hernia, the large distendedbelly. his face was a little bit larger than most boys his age. the geneticist recommendedthat we see a metabolism specialist right away, and we were able to go into that appointmentand the doctor looked at us and said, "i know

what your son has. he has something calledhunter syndrome, otherwise knowns as mps ii. and your reaction at that moment?i was happy that i had a diagnosis. i was thinking that.but i was devastated to know that my son would suffer for a while with many different ailments,but as you can see, he's doing great. he's a typical 7-year-old and he's having a lotof fun. but the road is a long road. and doctor, let's talk about that road. threeyears to get a diagnosis, three years of a mother knowing something's not right here.she gets the diagnosis. is jackson's history typical for patients with hunter syndrome?well, unfortunately it is typical that a patient sees multiple physicians, many doctor visitsfor a lot of different complaints until they

finally get that diagnosis. the specific combinationof findings varies quite a bit from child to child. but certainly that diagnostic odysseyof searching for a diagnosis is a very very common phenomenon.and carrie, obviously you're here today because we need to create that awareness and educateothers about this hunter syndrome. support groups? did they help you also once you gotthat diagnosis? most definitely. the support of your familyand friends is very important, but then we reached out right after that appointment andwe found a connection through the national mps society. they were a great resource forfamilies just to learn about the disease, but also to help you in this journey thatyou're taking. the website for that is www.mpssociety.org,

and just a tremendous amount of help for usa family. and doctor, what advice would you give toparents out there who may suspect that maybe their child has hunter syndrome?well, if there are multiple medical issues like we've been discussing, i would recommendthey talk to their pediatrician and seek consultation from a specialist like a geneticist. earlydiagnosis is so terribly important to ensure that a child gets the appropriate medicalcare. and do you have a websites for our viewersto learn more about it? medical information is available at a websitecalled hunterpatients.com. hunterpatients.com?yes.

carrie, for anyone out there who may be experiencingthis or may not know, what would you say? i would say please just follow your gut. gowith your instincts. you know, as a parent, that if something is just not right, searchuntil you find the answer. thank you so much for your time and for theeducation you've given us this morning. carrie, thank you so much for bringing your son andsharing his story. jackson, thank you so much. do you get along with your sister? that'sgood, too. thank you. god bless you. thank you, carrie. bye jackson. thank you.and for more information on managing hunter syndrome, please visit hunterpatients.comor our website, thebalancingact.com. (music).

(music).and now it's time to celebrate, and no one deserves a celebration more than the raredisease patients scattered around the world but bound together by their strength.there are about 7,000 rare genetic diseases that affect more than 30 million americansand millions more worldwide. the balancing act's behind the mystery series has highlightedmany of them. time is against them. it often takes over 7 years to reach a proper diagnosis,and an astounding 95% of rare diseases have no fda approved treatment. the global genessummit is out to change all of that through the global genes initiative. the 4th annualglobal genes rare patient advocacy summit and gala took place in beautiful huntingtonbeach, california. and this year hollywood

took note. it's the 2015 tribute to championsof hope. celebrity presenters included bryce dallashoward, jason ritter, and lindsey shaw. i am so happy to be here. rare disease awarenessis what's up. it's going to be a great night for learningand a great night for communities coming together and supporting each other.rare disease patient advocate and radio host, scott "froggy" langley played master of ceremoniesfor the evenings festivities, and american idol season 8 winner and platinum recordingartist, kris allen took the stage with 12-year-old global patient ambassador honorary, ben lou,for a very special performance. in all, more than 800 patents, philanthropists, advocacyleaders, and celebrities came together to

raise over $1.2 million dollars for rare diseaseresearch, education, and patient support. what global genes is really working to accomplishis to bring this community together to create a support network that expands beyond thedisease, and it's an honor to be working with all of those affected by rare disease thatare just incredibly courageous. (cheers and applause).to get involved, donate, or join the rare disease community, simply logon to globalgenes.orgfor more information. (music).we want to leave you with a few great resources for rare disease awareness and advocacy today.and we hope you've been inspired to support these brave patients and caregivers in theirfight to survive.

and don't forget to logon to thebalancingact.comfor all these great stories. you can also always follow us on facebookand twitter. remember, find your balance. so long everybody.(music). wardrobe provided by stage stores.

How to cure asthma who have severe

if everybody's ready i'm gonna go ahead andget started i don't know if everybody's here yet but i'm it is a little after 6 so i guess weshould get moving so i want to thank everybody forcoming to the talk um, i am christina johnston i'm a neurologist that work that works atlakeshore health partners on i've been the in town practicing for thepast year so i've sort of met quite a few patients with ms in my first year ofpractice and

i was asked to do a talk to thecommunity about a common problem that i've seen so far and ms was like thefirst thing that popped into my head i thought um, there would probably be somequestions and things that um, there's been some new medicationsthat have come out over the past few years so i thought it would be a reasonable thing to review just kind of do an overview of what is ms uh what are the symptoms of ms, howdo we diagnose ms and then some of the newer therapiesthat have come out over the past few

years i wanted to kind of touch base on those and then will beplenty of time for questions at the and i didn't get really really specific abouta lot of things cause i knew there was going to be probably a lot a questions so um but we'll have plenty of time forthat at the end okay also i wanna apologize ahead of time ihave a cough drop in my mouth cause i'm getting over bronchitis so i apologize in advance um

okay so i have nothing to disclose i'm independently employed i don't work foranybody else except for lhp so just want to get that out of the way ahead of time so what is ms what happens with ms? um ms is a chronic disease in the that affects thecentral nervous system that means that the brain the spinalcord and also the optic nerves which are the nerves that project to the eye and allow us to see can be involved in thisprocess

um, everyone has an immune system thatnormally fights of diseases such as bacteria and viruses any sort of infection and we think that the reason ms occurs is becausethere's a sort of case of mistaken identity that the immune system mistakes the central nervous system as a foreign object or foreign being and itunfortunately attacks it and creates a problem so statisticallyspeaking everybody likes to talk about statistics a little bit to get a generalidea

of how big of a problem this theis in terms of our country um it affects approximatelythe statistics vary a little bit but around 350 to 500 thousand so um people in just the unitedstates alone worldwide there's over two and a half million individuals and the estimate that in in the unitedstates alone approximately 200 people per week are diagnosed with this diseaseso it is rather common um more so than a lot ofneurologic diseases and its probably affected a lot of

i means i'm sure a lot of people up herein this room are affected but even in the general community most of uscan say that we know someone or or know of someone that has or um a family member who is affected by msor a friend or something it's very very commonly seen. um, it typicallyaffects males less than females i we don't really knowunderstand why that is but the ratio is about two to three females to one male um but that's kinda what wesee typically caucasians are affected morepredominantly

um than african-americans althoughcaucasians african-americans and hispanics are the most commonly affected we don'talways see it as much in asians although it can occur and there's a few other ethnicities thisis not as common um children can be affected by thisdisease although it's very rare in my training i did see i a fewchildren that were affected but mostly it occurs in our younger years it kind of the the sayingis that it affects a person when they're

in the prime of their life theirtwenties or thirties or forties or fifties when they're really you know doing greatthey're living their life they're having children they're getting married and this happened so it tends to occur kind of in the northernareas of the world the united states predominately inthe united states it's even more in the upper portions of thecountry as you get more south it doesn't seem to be as prevalent andthat's the case across the world so

europe japan some of those areas are moreoften effected northern european countriesspecifically tend to have a higher predominance of ms as well we're not really sure what that is theresome theories about that vitamin d or sunlight exposurecould be playing a role in why that occurs more commonly than nearer to theequator because it's very infrequently seen in the countries that are closer to the equator the life span a person with ms is

generally about on the average only afew years shorter than the normal life span of atypical american so you know people who are diagnosed withms still live a full life only they have to sort of um deal with thesymptoms and the chronicity of this disease so we still haven't identified exactlywhat the cause of the disease is but there's a lotta research so i just put this slide in because thisis i found this on-line and it's a picture above many famous faces

who have been affected by ms i think that's teri garr annette funicello who just passedaway she was seventy years old so she lived a long time with ms richardpryor ann romney was in the news with the lastelection kinda brought a lot of attention toward ms and raised a lot of questions about itmeredith vieira's husband i think richard cohen is his name he'sum a famous individual who's been in thenews a lot about you know what

attention toward ms and jackosbourne was diagnosed a few years ago so he's been in a few newspapers and magazines over thepast year so that i've seen so but it is it does affect anybody so so getting into a little bit moredetail about specifically what is it so everyone's brain and spinal cordare you know consist of nerves and thenerves are lined by a protective barrier called the myelinsheath so the analogy that we use is

that it's like an electrical cord with a protective you know insulation around the cord and that's the case withthe nerve so what happens is that the normalnervous system connects the brain to the spinal cord tothe nerves in the extremities which connects with the muscle andallows us to do things like move walk feel a sensation uh, visualize theworld so when the immune system attacksthe the myelin or the covering up the nerveit creates a disruption in the signal

transmission and so the signals can't get from the brainto the leg or to whatever is affected and it creates a problem so it usually happens when inflamation occurs after the attck of the immune system on the myelin so what happens with that is an attack aclinical attack a relapse a flare whatever term you choose to use our or yourneurologist uses to use but that's what it is so it's a suddenonset of neurologic

sometimes meaning weakness numbnessanything like that that comes on and doesn't go away for atleast 24 hours for some people it lasts for you know 3-4 daysfor some people it lasts several weeks and some people never i mean it canpersist longer so typically though that's not the casetypically it's a short term a few days a few weeks and then itgradually starts to improve which is why i sort of people can havesymptoms and then they get better and they ignore it and they don't even knowthat they have symptoms of ms. oftentimes ithappens to a 24-year-old 25-year-old you

know a young person they get better and they don't thinkanything of it until something happens later so that's the classic pattern that we here of relapsing remitting so a relapse followed by a remissionmeaning healing and going on with normalactivity so the symptoms can come on later inlife usually in this in the setting upinfection if we're stressed out if we're tired

and it's the result of the sclerosis left on the brain or the sclerosis just means a scar soafter the brain is attacked or there's a damage tothe nerve there's a scar that forms as it healsbut that scar doesn't have the same capacity that ithad prior to its damage so it can leave residualsymptoms going forward. over the course of one'slifetime you can see a decline in physical activity you can see a declinein cognitive ability so there are some chronic components tothis disease which is what

leads to the disability component you know and and managing thesechronic symptoms is you know that's my job that's what theneurologist sort of managers and and deals withon a routine basis so i put an illustration in here and actuallytried to put into my slide but it didn't work soi'm gonna actually just go to the youtube website it's not my video but i found it onlineand i thought it was a fantastic illustration

of the pathology that justtried to explain multiple sclerosis, ms is a disease thataffects the central nervous system the cns which consists of the brainspinal cord and optic nerves everything we do whether it's taking a step, solving aproblem or simply breathing relies on the proper functioning of thecns to understand how ms may impactthe cns we must explore the disease at thecellular level in the brain millions of nerve cellscalled neurons continually send and

receive signals each signal is a minute but necessarypart of intricate cns orchestrations thatculminate in the actions sensations thoughts andemotions the comprise the human experience normally the path over which a nervesignal travels is protected by a type of insulation calledmyelin sheath this insulation is essential for nervesignals to reach their target in ms the myelin sheath is eroded

and the underlying wire like nerve fiberis also damaged. this leads to a breakdown inthe ability of the nerve cells to transmit signals it is believed that the loss of myelinis the result of mistake in attacks by immune cells immune cells protect the body againstforeign substances such as bacteria and viruses but in ms something goes awry immune cellsinfiltrate the brain and spinal cord seek out the myelin

and attack as ongoing inflammation andtissue damage occurs nerve signals are disrupted this causesunpredictable symptoms that can range from numbness or tingling to blindness andparalysis these losses may be temporary orpermanent that was a really nice illustration ofwhat i tried to explain but obviously i can't do the video as nicely that explained itbut i thought that was a good explanation sort of of what thephysiology of ms is just so that you can

all understand if you weren't aware already so again why does it happen we don't reallyknow there's a lot of theories out there there's been a lot ofinvestigations about what specifically causes it because for for like i said it affects us at ayounger age so there's a theory that it's gotta be viral i mean we're all exposed to varyingviruses throughout our lifetime the one that's most commonly thrownout there is the epstein bar

virus which many of us were exposed toin childhood some of us were affected and got mono from it some of us hadno symptoms of it and they think it could be contributing or have some some role in making the immunesystem go awry and creates this this disorder as i stated earlier vitamin d hasrecently become a sort of big focus of ms and especially in preventingrelapses because we we think that low vitamin d levelslow sunlight exposure kinda that northern latitude

thing that i talked about beforethat that has some implication in in the relapse in and the and the incidence of worsening disease so there's a lot ofresearch going on in that and a lot of physicians now are starting to monitorvitamin d levels and if they're low which most people inmichigan have a low vitamin d level we're starting to replace it and kind ofget those level up a little bit into a more therapeuticrange because we think it'll help genetics is also something thatthey're looking into it can run in families

there's definitely a large number of you know families that do have msthat runs in the family but they haven't identified a specific genetic linkage i mean i have a number of patients in mypractice in my training i saw a lot of people that you know their parent was diagnosedor they had a sibling who had been diagnosed with ms so it it seems like it has some sort ofgenetic linkage but we just haven't really identified it yet

so ms is a broad diagnosis there are four typesof ms. the most common and the most significantly more common is the relapsing-remitting multiple sclerosis that affects about eighty-five percentof people who are affected by ms it's clearly the most common a much much less common is a primaryprogressive multiple sclerosis i'm not going to spend a lot of time onthat one or any of the others because it just it's not as commonly seen butprimary progressive multiple sclerosis

you don't really see the relapses the patients who are affected by that they they get a symptom and they don'trecover from it so there continue anytime that they havea new attack on their system they just continually decline but they don't havelike an outward attack and then recovery so it's a little bit differentand we think it might be a little bit thethe physiology of it is obviously a little different we haven't clearlyidentified that either there are not as many therereally aren't any therapies for that type of ms either and relapsingremitting

multiple sclerosis does have a number of therapies so i wanted to really focus on that type for this talk secondary progressive multiplesclerosis is kinda something that you see later in life in the disease processafter you know you've had it for a numberyears you start to sort of not have as many relapses or not as often and and things just start to quietdown or they seem like they quiet down but what we know about that is that inthat stage the relapses become less

prominent but the disability part seems to become more evident so thescarring on the brain that occurred earlier in life now starts to affect us more seriously and then progressive relapsingmultiple sclerosis is very for a rare but it is a is a conditionwhere there's a progressive componentthat can have relapses but that you know you you have a relapse but you don'tcompletely recover and it's more profound

than in relapsing-remitting so it's a littletricky to diagnose you don't see that one as often either this is sort of a illustration of the the type that i just described this oneat the very top here is called benign multiple sclerosisthat you know it it we don't see thatone a whole whole lot there's a very few people that have multiple sclerosis but they the completely return back tonormal and they just don't really

develop disability over their lifetime it definitely occurs it's just not ascommon and we don't we don't tend to focuson that one as much either those people are usually kinda groupedin with the relapsing-remitting because it is so soimilar there's relapses the disability just doesn't seem to beas profound but you can see with this illustrationwas trying to say is that with with each relapse there's a sort of apeak in disability the the y-axis here's the disabilityfactor this is time

so as our lifetime goes on there's a arelapse and we get better but if you notice youdon't completely return to baseline you may have a teensy bit of aresidual weakness or whatever your disability is and then a few years go by and then youhave another relapse and maybe you still don't return exactly to that baseline atyou are at and as it goes on it's just a little bitgradual progression of the disability component with primary progressive as i said there'sjust really no relapses there's

just a continual steady increase in theamount of disability over time but you just don't seethose peaks in sudden onset of symptoms the secondary progressive form here isvery similar but as i said there's just a much more you know a much less recovery to to the baseline there and it just as youget later in life to even the relapses become less prominentso and then this is the progressiverelapsing

so symptoms i mean everybody wants knowwhat are the symptoms i think so many people in my office who come and say i think i have ms i've been readingon the internet i think i have ms please tell me i don't have ms. i can't tell you how many times i seethat and then there are the people that come in they possibly do have ms so how how do we how does theneurologist know well i mean obviously this is a greatillustration because it shows that it

affects every part of the body essentially oftentimes initial symptoms canconsist of loss of vision in one eye or optic neuritis sudden wake up onemorning can't see out of an eye pain painful vision gradually progressesover a few days and then after a few weeks starts toreturn that's very commonly seen as one of the initial symptoms of ms it can vary though i mean some peoplecan have episodes of double vision or sudden

imbalance but as i said earlier in thetalk but symptoms have to be sorta consistent and last for more than 24hours so when people come to me and say i woke up this morning my leg is numband later in the afternoon it back to normal that's not ms okay certainly sensation can be affected numbness paresthesias meaning tingling burningthat type of thing that can that can definitely be msbut it's not something that you know we wake up with in the morning and it'sbetter by afternoon

that's different weakness oftentimes the initial symptoms orlater symptoms of a relapse or weakness that affects a limb you know my arm is all the sudden clumsier orheavier than it used to be and it's just not getting better and i think something's wrong its it's aprofound neurologic symptom that doesn't get better or doesn't get betterright away okay with the spinal cord involvement you can see things likebowel and bladder dysfunction

urinary incontinence urinary urgency having to go all the time difficultyemptying things of that nature. it can affectour swallowing it can affect our speech it can affect our cognition arefocus our mood are energy level i mean everyone who hasms the most common complaint is fatigue. i'mtired i have no energy i have to take a nap every day becauseit's just it wipes you out so these are the symptoms but it's theway the symptoms present and the duration and

and that that really helps theneurologist to to hone in on this could possibly be an ms symptom. so as i said when someone comes to meand they want to know how do i know if i have ms a neurologist is gonna really you know teasethrough the details of the history the history to aneurologist is the most important thing because i wanna know what is happening right nowbut i also want to know what has happened before

i mean what in your earlier you knowyears have you presented with or have you had and yourignored it because it got better you didn't think anything of it um the timing of it as i said how longdoes it last how when did it go away. has it ever comeback um that's really really critical tomaking a diagnosis the neurologic exam is obviously veryimportant um and can only you know a neurologistis probably the only one who can do it very well

um it's a challenging thing to do umthe imaging of the brain and spinal cord is very important before we had mri ms was much moredifficult to diagnose because we didn't have specific pictures wherewe could see the lesion or the inflamation or the attack um sometimes now less commonly we we still do a spinal tap to make ananalysis of the spinal fluid and see that there's evidence and inflamation but thirty years ago anyone who possiblyhad ms

got a spinal tap nowadays that's notnecessarily the case mri has significantly brought us muchmore advanced and we don't always have to dothat now evoked potentials which are the visual um the visual testing to see ifanyone's had optic neuritis i mean we used to have to do thosethings to really solidify a diagnosis and sometimes we didn't know sometimeswe had to wait now we sometimes may have to wait alittle bit to see if there is another relapse or see if there are new symptomsthat develop

but most of the time or very very often we can figure it out rather quicklybecause i technology has advanced so much but again i do see people sometimes where i say this is a clinically isolated syndrome you have a high likelihood of developingms based on your symptoms based on your imaging but it's not ams yet because they're very strict criteria that a neurologist uses and i'm not going to get into all that cause it's really boringand so this is a typical mri of apatient who's been affected by ms.

so i have two views here um this is asagittal image and this is an axial image of a typical mri so what we're seeing here is these areas here here here here sort of along the middle of thebrain this is the these are the eyes here this is the back of the head the spinal cord starting to develop downhere so we're as a neurologist, we look kinda alongthe center of the brain where ms likes to hang out

it tends to affect the portions near tothe ventricle which is this portion here and these are the ventricles here andhere as well and in both images you see these areas of inflamation these bright spots on the brain and theyreally like to hang out near the ventricles we don't know why but um that's the sort of classic picture of what an ms brain looks likethese areas where the inflammation is located is probably when arelapse occurred so we like to monitor mri's going downthe road after a diagnosis is made

to monitor the progression of thedisease to monitor if the the medication that you're on isworking it really provides a lot of information this is a picture of a spinal cord that has um a lesion on it so kinda just ageneral illustration of what we're looking forwhen a neurologist orders an mri that's why we want to get so what do we do for treatment umthere's no cure but we have significantly advanced intherapies over the last twenty years

um there's at this time still enormousamount of research in ms, um, they as i said in the last three years there'sbeen three new therapies that have come out which i'll talk about in a few minutes um there's a lot of drug trials goingon right now there's clinical trials there's you know in the lab trials going on andwe're moving very much toward toward um you know better therapies and therapies that areworking much much

um stronger at reducing relapses andminimizing disability which is really important so obviously though it's still abalancing act because we have to maintain our immune system and find atherapy that allows our immune system to be suppressed enough so that it's notgoing to continue to attack itself so it is rather challenging and that'swhy it's taken so long to get to where we are now wehave therapies available that work with minimal side effects and um you know that you can be on for a long along period of time

so the treatments that we do haveavailable obviously the acute relapse is when something happens most the the themainstay is steroids it still is it was fifty years ago um when you havean acute relapse if anyone has ever um had a relapsesteroids are kinda the mainstay it ek expedites the healing process it doesn'tcure anything but we want to get you back to your baseline as soon as quickly as possible and get you backon back on your feet. um, the diseasemodifying therapies are the ones that i'm gonna spend most my time talkingabout and the symptomatic therapies um

i'll touch on a little bit but that'sreally individual so you know based on what your symptoms arethere's there's multiple treatment options but it's sort a veryindividualized so in 1993 was the first um disease modifying therapy that cameout it was betaseron it was an enormous breakthrough for mspatients because all the sudden there was something to put to be on to reduce the relapse rate andto reduce the potential of of progressing withdisability

um since since that time so in 20 years we've come up with 8 fda-approveddisease-modifying therapies actually i think there's actually 9 butone of them i didn't include because i don't see people using it much anymorebecause it has a lot of bad side effects so kinda moving away from that one sincewe've gotten some newer ones um ah all of the disease modifying therapiesthat are on the market um have been shown to reduce relapsesmost of them have been shown to at least reduce the progression of disabilityand many of them have

have also been shown to reduce the thenew lesions seen on the mris that we that we periodically check so most of the actually all the therapies are generally safe and well tolerated when i say generally there are a few um significant complications withseveral of the therapies that we very closely monitor and we look out for and and we're very on top of those ah potential risks so we'll talk about that um on avaerage the injectable disease modifying therapies have been shown to reducerelapes by 30 percent

the injectable um have been around the longest um only in the last three years are therepills available now so most people who have had ms this long have been on injectabletherapies of some kind um all have an anti-inflammatoryeffect on the immune system so reducing inflammation bringing theimmune system down to a more manageable level and reducing the relapses um most of thetherapies require some kind of blood monitoring

there are a few that don't require as much butthere are you know a maintenance test that oftentimes have to be done to ensurethat it is it safe to continue beyond so the first category is that i'm gonnatalk about are the interferons interferons are normally present in our immune system and betaseron is the first one thatcame out it's also called extavia it's believed to suppress the movement of t cells which are a typeof immunecell across the blood-brain barrier sothere's a there's a wall between like

the the blood flow and the brains cellsthemselves and so the immune cells have to sort of transpose across that and invade thebrain to cause the attack so this medicationwas aimed at reducing that transposition ofthe t cells across the barrier the barrier into the brain this is aninjectable medication every other day it's been around the longest there'sbeen a lot of people who are on it at first and then since that came out there's afew others that have come out as well in

the same category it's approved for relapsing-remittingmultiple sclerosis it as i said reduces relapse and byabout thirty percent so it's a pretty reasonable numberit does have the unfortunate side effect of them flu-like side effects with the injectables but um for its different for everybody and wehave you know wonderful nurses that we you know use totrain our patients to help sort of minimize those unfortunate side effects

um interferon um beta-1a are the avonex and the rebif this isthe same medication but in a different form in a little bit different dose so avonex is a is a once-weeklyinjection um it reduces relapses as i said byabout thirty percent as well all the interferons are about the same interms of numbers it's been shown to slow disabilityprogression which betaseron did not and also reduce the mri leasions that are seen

mmm so avonex is once a week rebif isthree times per week under the skin both have flu-like side effects unfortunately but as i said for most people it'susually worse in the beginning when you're starting the therapy as you sort of get established on thetherapy the flu-like side effects do tend to dissipate and you sort of learn how to how to manageit you pick a day that sorta works for you that you're able to be a little under the weather and stillkinda go on with your day to day

functioning with both of these medications um bloodmonitoring is required you have to monitor the lever we monitor the the the white count to make sure thatyou still have a good immune system in that the platelets and other things haven'tdropped so we do do periodic blood monitoring with the both of thesemedications the other injectable medication is glatiramer acetate or copaxone copaxone is a different category ofmedication that's not an interferon

its actually a combination of aminoacids that are believed to be found in the themyelin or the on the a it resemble the mylan and itsupposed to suppress the t cells and reduce inflammation um it's approved for relapsing-remitting multiple sclerosis as well it does also have a 30 percentreduction in relapse rate it has not been shown to decreasedisability

um but it is widely prescribed it everyday under the skin it has very minimalside effect it has no flu-like side effects it is tolerated by most people who dothe injections and its kind this is the one i kinda tellpeople it's like being a diabetic you sort of just do your shot every day and you justgo on with your your day so this is one that'sbeen very widely prescribed for women who want to have children it'ssafe during pregnancy this is the only

one that has been shown to be safe for pregnancyfor women that are in their childbearing years andaffected by ms this is one that is often used because you know you don'thave to go off of it you don't have to go back on it for some of these medicationsit takes several months before they reach full effectiveness so that's a nice that's a nice perk tysabri is a once-a-month infusion tysabri is a very wonderful drug when itcame on the market it was like the breakthrough it was i believe 2007 ihave to look that up specifically but

it may have been 2007 when it came onto the market and it was pulled from the market a yearlater because of an infection of the brain that was foundto occur called pml pml is a viral infection that isirreversible and it can result in death it canresult in very significant disability and it is not taken lightlyby any neurologist it is a wonderful drug now in the sensethat it's once a month you go for your fusion yougo home and that's it for the month and you feel great and there's no sideeffect and its a fantastic option

but it has very specific protocol that has to be very closely adhered toonly approved neurologists and approved centers canadminister this medication you have to have very strict criteria with every infusion you have to havea patient who is incredibly willing to adhere to the rules and it it is very closely monitored but it has a reductionrelapses of by about 67 percent so far surpasses all the other ones

it slows disability progression andreduces the mri lesion and it's a great drug but i'll tell youhave seen pml and it's not great it's horrible itkills people its it is worse than ms so that's why we don't we don't pick thisfor every person with ms this is a medication thatis reserved for patients who have failed other therapies and are havingprogression and we need to do something stronger but it's a great drug

yes when it is used yes as is the case with some ofthese other medications that we'll talk about so these are the new oral therapies so anyother a 50 and tech for their of health which is awesome no injectionmany more so don't wanna make you mine in 2010 it's a once-a-day tablet it has areduction in relapse is about fifty percent

but unfortunately this one has um someunfortunate cardiac side effect that we have to really closely monitored there have been some reports of suddencardiac death with this medication so we have to pick patient to have no history of cardiac problems arevery minimal risk risk of cardiac disease on it has it produces a disease progressionit reduces mri region on it up believed to keep the lymphocytes inside the lymph nodes andprevent them from

i'm going to go to the brain so that'show we think it works i'm this one can also affect our visionin 'cause a macular degeneration so that's something that has to be screenwhile on this medication on there's a little bit of bloodmonitoring of the screen for z/os oster or her on that shingles by rest but its job it's a good medicine to it's been outfor three almost three years now and there's a number people on it andthey're doing great sold that was the first one

i last follow by your weather pro why wealways called theraflu my careful in mind is a agent that has beeni around for i'm not not here for thenight um left phone in my which is anotherderivative i love up here for the night or similar has been around for much longer so we dohave some information about this on similar products and it was approved as a once-a-day tab what you is believedto have hit a flamer three properties that reduce the lymphocytes and the

in the central nervous system thespecific seven or a little little sticky to me i don't completelyunderstand that exactly but its i'm it's been around and it'sstarting to be prescribed more commonly on it has a specific similar with theinjectables about 30 percent i'm however the big the big fancystatistic here is that eighty percent left new lesions on mri which is youknow a really important i factor for forpatients this is %uh pregnancy category axoanyone who's in there childbearing age range is probably notgoing to be a good candidate for this

medication because it's very risky i'm category act in the medical worldmean absolutely not cannot get pregnant onthis medication even males who on could potentiallyimpregnate their wives are supposed to be warned about that because that's beenfound from and also to be a problem so we haveto monitor blood pressure and we have to do a tv screen but this is a once-a-daymedication that is an option for people if you're me onyour childbearing years and it's okay to be on something like this

than this is a great option i i mean i'm i'm really excited about the final southi'm and tech for there is the most recent one that just came out a fewmonths ago it's a twice-a-day medication it has alittle bit different i'm back in them mechanism of action apredominately work from the anti-oxidant pathway from which is kinda a new thing i meanwe vote we always hear about anti-oxidant thing as both a drink all these and accident you know throughyou said that thing for

it that there there is a lot of ongoingresearch in this area so there's probably going to be more drugs in thefuture coming out in the area this heather a reduction relaxes by of53 percent on disability is also decreased by 38percent the side effect prior profile is prettygood i mean it it does cost them flashing for people the face feel a little hotfor about an hour so after your does tends to get better after about an hourfrom what i'm told and tends to minimize over the course ofthe first few

first few weeks by the end of the firstmonth and told that much better i'm it can cause an upset stomach somegastrointestinal discomfort but its sounds like a great drug alsovery little fight a fact starting to see i mean i have a couplepeople are there now i haven't heard a lot about feedback fell i've talked with some colleagues whothink it's great i worked in a center that this was a medication on in the research trial i so great great day out on the fun thismedication was available

in europe for psoriasis so it's been onthe market for a long long time and they have a lot of good data thatits safe and effective of l so this is a great option for people so with all these nomads how did theneurologist user how does the patient on you know how do they know if theircandidate for these new medications well that's complicated a little bit armyou know for patients that have been stable on their injectablemedications it's really hard to to take them off abit right away knowing that they're doing so while

for patients who have horrible sideeffects they've been he never have an accident when he nearly there forwhatever the case maybe they had their compactness and the they just have had horribletolerability issue 3 years and now these pills are available i mean that's areasonable option but it's very individualized with eachcase scenario its it differ on thought process into why would weswitch for some people they they do fine airduct herbal medications but they're just getting worse

and they need something different andthese are available and they have a different mechanism action so it's a different way offighting of immune system so that's a reason to pick it for some people they have no symptomsbut there are my eyes are looking worth and something needs to be done so thatdisease progression or disability doesn't occur in 10 years so i mean there are a lot of thoughtsthat go into a neurologist mind when we meet with you every visit to talk totalk about your therapy

i'm it's not an easy choice on it's it's a it's a big it's a bigdecision to switch therapies and there's risk with which in therapyand their side effects were searching therapy so is very individualized anyone knowthem if they know all about the the risks of medication and it'sit's a case by case decision so what if i for one person thenecessary pie for the next person so what if you think you have an ass orwhat if you know somebody who that you are concerned might have my math the tosee somebody about it they need to get

evaluated by a neurologist somebody whois familiar with a mass who can really look into it on becausewhat we know about a mass and what we've seen even before before i was even born and31 years old well i mean this has been a long foraround for a long time and you know my trainers have been doingthis for a long time they saw people when there was nothingto do and every year things got worse but now withtherapy things slow down and and people areliving longer with left disability with

more functionality there no one not me it's now they have amassedbecause they can you know have less and less symptoms as they'relike 10 cause on and if you don't get treatment as soon as possible or as early as you can then the risk forrelapse is increase as and with that is disability so theearlier you're suspecting sometimes the girl you should see somebody inc andfigure it out for people who have been diagnosed withms and have been living with us for years that the whole different you knowit's a different ballgame

arm the symptomatic therapies are as isaid earlier very individualized there's plenty of medications out there to treat the fatigue to treat thespecificity to treat the depression to treat the bladder problems to you know i mean there's there's lotsof things that we have in its obviously with one thing is that work we trysomething out then if you know something doesn't work we stick with it but its its it depends on the same foundit depends on the person but i'm you know that's a conversationyou have with your neurologist

so when when a piece with a mask onthrough my office and i see them and i say howare you doing me not the time to say all my fightersfiring me or are not sleeping or how or and on thetop i mean because thats that the conversation thatyou have with your neurologist is how are you doing mean when when iwalk in there are many say how are you know that's what i'm i'm great but i'm thesafari me i mean that's what the neurologist newsnow that's how we decide how to treat

your symptoms and what to change in what to dodifferently so physical therapy is a great optionoccupational therapy for people who have you know you know different i mean it'sdifferent for everybody but those are great resource to the physical therapist in this town areawesome their top-notch i've sold many greatresponses from people that have gone physical therapy for youknow not just amassed we have a really great

i'm community with wonderful resource sso i find take advantage of that term in patients and i always make that an option on assistive devicessometimes are very helpful for you know foot drop or whatever the casemay be on you know when upper extremities arespastic and it's hard to go grab things are open jars and its its there's things available forthat so you have to talk to neurologist about it so that we can get get to the healthyyou need

living environment something had to bechanged living in a house that doesn't have a ton affairs you know bathroom accommodation thingslike that so that we can minimize complications exercise is always you know i never tellthem not to exercise i mean there's out there different degrees of exercisersdifferent things to do exercise is really important healthydiet good sleep home you know stuff stressmanagement hard stress management is something that andthe doctor can preach to you and any

person can preach to you but it you know i mean every person hasstress and everyone deals with it differently but it is important because when you'remore stressed your symptoms are accentuated and it's really important tosort of keep that under control and if you're struggling with that toask for help support refer great till i'm for porkribs are wonderful in the sense that they can give you someone from listen to yourstruggle

and also you know here what other peoplehave gone through it it's wonderful in some cases they can make you a littlenervous that oh my gosh i am i gonna be in a wheelchair because that's the mostcommon fear everybody and and i will tell you it'snot it's getting better i mean people are doing better forlonger with the advancement a medication so i thinkthe people that are weird wheelchairs thirty years ago if they were to havebeen diagnosed now maybe wouldn't be in a wheelchair asfeeling or maybe not ever its it's two things have changed andthings have advance and we definitely

are making a lot of strides so i put the fight in here actually wehave a handout over here with this information so these are justsome wonderful online resources that of anybody familiar with them but thenational ms society is a fantastic resource for helping with you know disabilitybenefits for insurance for work for all sorts of questions that we facein our day-to-day routine when you're living with a math i'mnamath lifelines them a active sources those are both onlineresources that can answer questions that

can provide i'm you know there's a mentor their i what i think both of themactually i must leave by the time as active force have resources to talk with a mentor ifyou need just somebody to talk to or someone who's been there there therethose resources there on the ms. foundation & spa sharedsolutions is great because they help with you know in questions at work questionsabout injectable therapies how to make

things better if you're struggling from they're they're wonderful ownersays that can provide way more our answers to questions that probably ican hit and fell i use them a lot self and on your side and i went a little bitover arm there's about 10 minutes left i'll have out safer any questions so i hopethat wasn't too boring or 200 perfect i okay thank you i

the the question why is on i hadmentioned some speech sometimes and the question was what would be somespeech something that frontal lobe lesions while i suppose that's a complicatedanswer as as is the case with most neurologyfrontal lobe lesions if they involve them older pathway can affect you know themechanics above the mouth so can make you have a more defarthritic or more about flirty your speech

are making about the throat so couldhave more modest phonic or some kind of like problem i know how to explain that very well butit it can make your your speech down a little thicker because thethe vocal cords and the the the throat doesn't move as nice andeasy as it use to sell i'm that would be the most obvious thingi would think of so the question i was in the videopresentation there was a comment about how the the pathway or about the pathophysiologyof an ass is that detects the mylan

but also that attacks the nerve fiberitself meaning axe on and that is true what we learned about our math with mriis that when the mylan is damaged the accentbeneath it can start to wither away because it isthat we don't know why that happens but probably because it isn't protectedas well and so the signal isn't being train ducted as well and the nervestarts to die of a little bit and we know that because i'm mri we seethese black holes is what they're called buttheir holes

in the brain that occur almost on a bitlike a stroke but it's not a stroke it's completely different ideology but it's a hole where the the nerveitself has basically sort of deteriorated we didn't really know that until mri sothe theory has changed a little bit and that's where we think the diseasedisability long term comes from is when those black hole or the the axeon itself has started to be this integrated oraffected is when the the secondary progressive disease comethen we've only learned that over the

past twenty years but you it without contrast it's actually i'm aon the t1 sequences which i'm i have many sequences that we lookat and when we're looking for active information we always look at the flarefake ones are the key to flare sequence that those were the sequence as shown inthe images during this presentation but they're also the sequence called t1and that does demonstrate the black hole so we don't see it an early amassed wesee then later on that

cell but yes that's a wonderful questionwe didn't know that for a long time i'm the question foreverybody is does the number i've lesions on mricorrelate with the number relapses or the number are the severity ofdisability i got answer is no i'm there are mri's they look horrible like the 1i showedyou i've no idea that beijing was i i just picked that picture because ithought it was a good illustration but mri can be horribly deceiving and look where the like that and havevery few clinical symptoms

okay the opposite case can occur whenthe brain never really look that bad but the location of the lesion can be inthat specific precise location that it put leaves you with a lot a disability so patients who havebrain stem or spinal cord lesions and not a lot inthe outer portions of the brain can have a lot of disability in lifereally bad and their brain doesn't look that bad so it doesn't always correlate but the reason we monitor mri is becausewe wanna see is there any new

regions that have had some sort ofclinical correlation because there is a silent component andmath because every new lease and doesn't always have a symptom so not in my training are not in my career time i'm i get a repeat didn'thear the question on can we use combination therapy toimprove the immune system fight against i mathi'm the reason the answers now we don't dothat i'm and the reason is because for example in

the i text every trial those patients that developed p.m. i'll were alsoanother 30 some of them have been on avonex okay and some of them have been on otherchemotherapy drugs for other conditions and we think that that significantlyincreases the risk of infection and so we're incredibly leary i'veexposing people to too many infections because brain infections are veryserious so we don't take that lightly and most of the studies are are comparedagainst placebo

on there's very few trial to comparehead to head against another product but they do not allow people to be instudies with combination therapy for that reason because i've the risk ofinfection so it ecological box and a lot of peoplehave discussed that but in my training in my career and eveni think in the twenty years that they've beenavailable people are just not doing that i mean i've i've not seen that anywhere cell and in fact sometimes when we takepeople off medication and what's worse is something differentwe give them a little bit of a washout

period meaning some time to get that drive outother system so that that is not a risk exercise for that's great it's mentally therapeutic it obviouslyvery you feel better and we think that keeps you a mandatoryfor longer felt thank you that that's great can you still have amass if you don't have lesions on your brain probably not okay that i am there is a condition called honor mylatest after car which is a very into a

mass it's not an ass but it is usuallyconsist of spinal cord lesions with no liens on the brain and opticnerve so it's nerves on the eyes and spinal cord andnothing in the brain which it's very similar amassed but ifyou have a massive you have something on your bringing now in my opinion is in my opinion is a funbetter than vitamin d i'm i don't know the answer to that ithink it i think it might be i mean look at thepeople that live close to the equator

they don't have this problem see kinda wonder right but we don't havethat ability we'll we have you know how many month of cloudinessand no sunlight and it makes us all depressed and crankybut i mean it it does make you wonder bowlthat's all we have as the vitamin d3 for or a supplement inthis area the country's how often that's a hard question howoften it is is it in the arms versus the legs or probably refers tothe life versus the arms or both i'm i don't know that i've ever

paid attention to that truthfully ithink we notice when it's in the legs more of 10 because it affectstheir walking effects are emulation but the arms arenot taken lightly either i mean writing we are driving everything we do i mean idon't i don't really have an answer to that because i never really paidattention to watch is more prominent for a lot of people in effect 15 thebody so if the arm and a leg on one side for of but is it just one arm or justone lag i don't know which one mark on for andthis is a complicated disease because everybody's different not one singleperson with ms looks like the next

person it's very variable cell it which is thechallenge so that i thought he wants to knowbecause the location of the lesion that mri are so close to the ventricles in thecenter of the brain does that mean that there's somethinghaving to do with what we ingest into our bodies and that it's crossingthe blood-brain barrier somehow and affecting the brain in the centre portions fromsomething we ate

i don't know i i'm never heard back thatphiri inexpensive one for insurance is a lot of times are youknow people use their insurance if the payfor those expensive thing so that's why they hurts so much because insurancecompanies molpe the big box and if you don't haveinsurance or free insurance won't pay the static at the big bucks so i i truthfully i don't have enoughlot of knowledge about where that

cheapest devices are located i knowthere's just you know i i refer people to medical devicestores because every month options but i don't know that that you're rightthey're not they're not cheap it's such a in my practice i'm i don't want anyone i don't want anybodynot be on drug because they don't have insurance there are so many resources most ofthese drug companies will make sure you get the drug and andmost of them have assistance programs so that you can get it for free for ayear or two or you can pay

you have attend our copay or they almostall these drug companies bent over backwards to get you on their their therapies i meet my partnertrained in inner-city chicago in you know he he saw people who had nomoney no place to live and we're getting drugs so these drug companies will make surethat you can get therapy if you have a diagnosis so somebody who told me because they don'thave insurance enactment take their medication

i can i that's not enough for me me hi i really do work very hard to get peopleon therapy because i really strongly believe that you know idon't want to be disabled so i i want i want to make anyopportunity to keep you functional keep you livingas long as possible i think that's changing a lot now ithink one other one other company they know for sureabsolutely will pay for your dog if you can afford it and in fact actually to %uh the companythen oh well yes people with the

injectable the aft since the orals have come available imean i think i've only been here for a year okay so i've assumed a lot of people whohave been in this community and had a diagnosis and you know maybe they're just lookingfor a new neurologist so yeah people that i've had a long termdiagnosis and he did the injectables and couldn't deal with it both people have been offered drug itried to get them back on therapies

i really have because i'm especially forcoming in there are already using a cane or there already have been you know something going on or orthey're having relaxes and they're still me the biggest thing is clinically howare they doing it for not having relapses anymore and the baby there there stable or their may be progressing a little bityou know that's going to be a different situationbecause these medications are pro for relapsing forms

so on paper that is something we have tobe careful about because if you're not having relapses anymore it may not be covered cell these thesetherapies are only study in relapsing-remitting cases are notstudied in primary progressive they're not studying and secondary progressive so that's a little bit of anindividualized case as well but yeah if people have an offer theinjectable i am trying to get them back on yourtherapy is thank you so much to everyone okay

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second opinionepisode #903 foot pain announcer: major fundingfor "second opinion" is provided by the bluecrossand blueshield association, an association of independent, locally operated,and community-based blue cross and blue shield companies.for more than 80 years, blue cross and blue shield companieshave offered health care coverage in every zip codeacross the country

and supported programsthat improve the health and wellnessof individual members and their communities.the bluecross and blueshield association's mission isto make affordable health care available to all americans.news about our innovations is online at bcbs.com and on twitter@bcbsassociation. "second opinion" is producedin association with the university of rochester medical center,rochester, new york. salgo:

welcome to "second opinion,"where you get to see, firsthand, how some of thecountry's leading health care professionals tackle health issues that are importantto you. i'm your host, dr. peter salgo,and today we're happy to welcome physical, occupational, andmassage therapist boyd bender. our "second opinion" primarycare physician, dr. lisa harris. dr. judy baumhauer from theuniversity of rochester medical center.dr. douglas hale from the

foot and ankle center ofwashington. and dave heller, who's here toshare his case with us. by the way, this is a case thatour panelists, along with you at home, will be hearingfor the first time. so let's get right to work.dave, several years ago, you were training to go -- and i'mnot making this up -- an extreme elk hunt? heller correct, yes.and you had to hike in

60 miles. correct.you want to tell me about this? well, actually, a friend ofmine who lives in colorado, in the northwestern part, doesan annual elk hunt, where they go into federal lands and hikeall the way in and spend about ten days to two weeks.and in preparation, i decided to start working out -- probablyabout six months before the hunt.so, doing regular physical activity -- i am a plumbingcontractor -- i'm in pretty good

shape and decided that i neededto work on strength of my legs, as well as increasing mylung capacity, wind, because we'll be at 11,000 feet.so i started working out, and one of the workouts wason a treadmill, and i became quite proficient on thetreadmill and decided that i would put it on an inclineand then start to run on an incline on the treadmill.but the thing is that, with working out on this treadmill,after probably about 2â½ months or so, i suddenly got atremendous pain

in my right footand decided i should go to our local podiatrist and see what'sgoing on with the foot. now, had you -- well, first of all, what did the podiatrist tell you? well, he told me that i hadpinched a nerve in the front part of my foot,just below my toes. salgo all right, and had you everhad any foot problems

prior to that? actually, no.i was born flat-footed. i've worked in constructionsince i'm 14 years old, which includes jumping into deepexcavations and jumping off of scaffolding and ladders andtrucks and things like that. so i want to stop for aminute, because everybody i know has heard the phrase,"flat feet." we have a picture of a flatfoot. that's what a flat footlooks like.

what are we looking at?anybody want to help me out here? baumhauer well, it's a foot that issort of sagging in. we call it "pronating."and essentially, the structure of the foot is quite flat, so ifyou walked along the sand, instead of having a little archin your footprint in the sand, you'd notice your whole"flintstone" foot would be sitting there.so i want to talk about the

treadmill for one second.so, the treadmill, the repetitive, continued walking atthe exact same speed, with the exact same step,makes anybody who has any near foot problem vulnerable.it would be better to walk outside.change your terrain, change things around so that you're notdoing the exact same thing. harris: you actually havean abnormal gait on the treadmill because of thestructures in the front.

you change your natural gait,and we see a lot of problems that occur with people -- bender: well, also, peter,you've mentioned that he changed two variables at the same time.you increased the incline of the treadmill and then startedrunning, which can oftentimes cause a problem. hale: yeah, on a treadmillwith the elevation, your heel

cord gets tighter, your foot'sgoing to flatten out more, you're going to put a lot moreforce through your foot, also through the front of your ankleand your forefoot, with going on an incline on a treadmill. and now you've gotfoot pain. and somebody's told you you'vegot a pinched nerve. now, you're on your feet allday, and your feet are hurting. heller: correct.

what happened? i went to, again, a localfoot doctor, podiatrist, determined it was a pinchednerve in the front of the foot, which he gave me a shot ofcortisone, i believe, something like that, and said, "by theway, you have really flat feet." and i said, "yeah, i've beentold. i notice how my work boots wearout, you know, on an angle, and so forth, like that."and he said, "i'd really like to fit you with orthotics."

all right, so, let'sstop again. because you've seen yourpodiatrist. did your podiatrist get anyx rays, any studies? just looked at your foot? actually, he did x rays. i would ask, where were youhurting at, what location was your pain? the front part of my foot,just below my toes, was where most of the pain was.just in one foot at that

particular time. and was it continuous, orjust occurred when you were exercising? no, that was continuous --after i had done whatever damage i did, then that was it, thatwas start of. salgo: even at rest? yes. even sitting or lying inbed, it would hurt? it actually -- i guesssitting or laying in bed, it

wasn't bad, except when yougot up. then it was bad. okay, so, if someonecame into your office with foot pain, how would you work it up? well, the first thingis to get some of the history that we've already asked -- whatwere the activities? one other question would be,did you buy new shoes? or were you using older shoes?i'd want to examine the shoes that you brought inthat you were wearing during

your exerciseand the ones that you wear during the day.and then a good examination of the foot, including a sensoryexamination, so we would check to see if there was any loss ofsensation anywhere in the foot. i would do exactly that.i think every patient, you have to start with a good history.you can't do tunnel vision. you have to find out, do theyhave any arthritis themselves or in their family, any othermedical issues

you may be dealing with?and then every patient needs an excellent physical.so you need to look at their skin, you need to look at theirblood supply, you need to look at their nerve status.and then you need to do a good musculoskeletal examinationto find out exactly what structure is hurting, wherethey're hurting at, to make that diagnosis.so a diagnosis needs the proper exam to get that done. i would take it even furtherwith the physical examination.

with the complaint of just --the problem on the one side -- is, people always have a historyof old injuries, not just at the foot or ankle, butat the low back. and there could have beenan old disk injury that healed a long time ago, but now it'smanifesting itself in a way where there's a lot of weakenedmuscles in the lower leg, that may cause that foot toflatten more than it normally would. what i'm hearing is veryinteresting.

you've looked at the foot.but you've thought beyond the foot. you have to.to think of other things which might be impin-- that'svery interesting. impinging on the foot.would you do anything else? baumhauer: think what's interestingabout the story is, he says, "when i'm at rest, i'm doingbetter, and when i get up and use it, it hurts more."so i always think that's

mechanical foot pain.and not -- it takes me a little bit away from nerve pain. nerve, that's right. so i'm thinking more, it'sbones, joints, than the nerves, that are primarily the problem. all right.but dave gets cortisone and gets an orthotic.what's an orthotic? when do you prescribe it?what's it supposed to do? and, actually, i justwant to jump in with my

non-ortho expertise.starting an orthotic when he has acute foot painthat's unrelated to, you know, his flat feet.i'd want to take care of the current problem before i startedprescribing orthotics for a chronic problem. what is an orthotic? an orthotic is something thatyou apply to the bottom of the foot -- it can be dispensed overthe counter or custom-molded. it's an insert.

goes in the shoe.and it's supposed to straighten your gait and make everythingbetter. it's supposed to support thefoot in areas that require it, to try and decrease painor improve function. in his particular case,i'm not clear exactly what the ongoing diagnosis was, but i'msuspicious that they thought it was a neuromaor something like that, with that cortisone injectiondiscussion. and sometimes, anover-the-counter orthotic

with a little pad can help splaythe forefoot open a little bit and allow the nerves to be alittle less squished, if you will. but that's depending on thediagnosis of the nerve impingement.so the $64 trillion question in today's health care economy,how did those orthotics work out for you, dave? well, not well at all.i think the original, first set of orthotics -- by the way, theywere --

oh, i know we're going tohear about more. okay, made the pain better,worse? the pain got worse? what? well, the initial pain seemedlike it was improving. i mean, becoming less.but i don't think it had anything to do with theorthotics, because the orthotics weren't dealing with the initialreason why i went there. did your injectiontemporarily relieve your symptoms?

i had three differentinjections. but for, like, an hour afteryour injection, did your pain go away? it numbed it for a while.or it felt a little better. so, if you look at, if we doa diagnostic injection, whether it's on a joint or on a nerve,if your pain goes away 100% for an hour, there's a good chanceyou're at the right spot. if you inject a nerve and yousay, "my pain doesn't go away," it may be the joint that's atanother area of your forefoot.

so the big question is, doesthat diagnostic injection relieve your pain?'cause if it doesn't, maybe it's not the nerve, maybe it'syour joint. forefoot pain is commonlyjoint issues also. i'll back up on the orthoticissue -- so, a lot of people come in, they're not coming inbecause they feel fine. they're coming in because theyhave a foot-pain issue. so you're trying to help themresolve that problem. so the first thing to look at isshoes -- a lot of times, they're

wearing an unstable shoe.they're wearing a shoe that's not properly fitting for them.so it's giving them pain in a certain area because of theirshoe gear. so a lot of times, we can changethe shoe and make them much better.the other thing is an over-the-counter insert, and alot of times, we are rebalancing the forces in the foot.so we're using an over-the-counter insoleinitially to rebalance those forces, to move force to an areathat doesn't bother them.

now, i was listeningto you, dave -- i caught a whiff of, you went to the first one,you tried the orthotic, it really didn't work very well,time went by, i heard there was at least one other orthotic.was that with a second podiatrist? okay, and that didn't workvery well? that didn't work very well. salgo:so let me guess. you went to a third podiatrist.

went to a third.this particular foot specialist also did sports medicine, and heworked with a lot of people who ran marathons and thingslike that. so he agreed that yes, i haveflat feet, and yes, i could use orthotics.and of course the other ones were not properly administered.but in the meantime, he decided that i also had heel spurs. a bone spuron your heel? both feet.

in the interests ofeducating america, we've got a bone spur.can we put that up and have a look?there it is. what are we seeing here?somebody want to -- we're seeing a spur atthe bottom where you typically see plantar fasciitis. plantar fasciitis iswhere that fascia, some of the connective tissue in the foot,hooks on. so the connective tissue onthe bottom of the foot hooks on

and pulls, and you get thatspur. so we know heel spurs are commonwith aging, from studies. people who have heel pain have ahigher chance of having a heel spur.but you don't have to take the heel spur offto get them better. let's pause for a minute,because that's a heel. and if you follow the bottom,there's that little hook-y thing on the bottom.that's the bone spur. hale:correct.

salgo:and that hurts. harris:well...sometimes. it may or may not.may or may not. right, so gettingan x ray and seeing a bone spur does not translate intofoot pain. and the other thing is,patients should realize that you don't have to haveyour bone spur out. so 35% of people have an x rayjust like that and no pain whatsoever.so don't treat the x ray.

so bone spurs don'tnecessarily need treatment. bone spurs don't necessarilycause pain. just finding a bone spur on anx ray, dave, doesn't necessarily mean that's what's causing yourtrouble, correct? correct. however, i believethat, with wearing the orthotics, now both feet hurt.okay, remember, i started off with one foot with what ithought was a pinched nerve. now both feet hurt. so no good deedgoes unpunished.

by the time i got to thethird foot doctor, okay, he is now saying, "yes, they'reflat, yes, you need this, but you're also --" and i wasexperiencing pain in my heel. both heels.so this is when he determined that i had heel spurs. but there's no guarantee thatthat pain is from the spurs, is what i'm hearing from my panel. the spur is a secondary\thing, not a primary thing. what treatment did youget from your third doctor?

well, actually, i wenttwice a week for, i would say, five or six months, but therewas all types of, you know, certainly the whirlpool thing.you know, there was different types of stimulation. this is your area ofexpertise, isn't it? does this stuff work?there's massage and electric stimulation... it can work in the acutephase, but it's certainly not something that's going to healthe problem.

again, you have to get back towhat is causing the problem. okay, and all of these otherthings may be ways of treating it, initially. okay, so the acutephase means it can make you feel better, but it doesn'tnecessarily fix the problem. it does not fix the problem. when he'sfirst hurting. when you'refirst hurting. he's now intochronic pain.

you're now into –years into this. where did you go next? well, that particularspecialist finally decided that he could go no further with meand then recommended a rheumatoid guy.maybe i had some r.a. in my foot. "r.a." meaning"rheumatoid arthritis." meantime, you know,the foot -- both feet are now to the point where i'm kind ofhobbling a little bit.

i thinkwhere he's falling short -- so applying something to thebottom of his foot, sending him off to physical therapy,you know, we're all sort of questioning, where's thediagnosis, and where is it going?you know, there are a lot of options here.if in fact you had heel spurs, plantar fasciitis, if in factthat was the case, you know, the mainstay of treatment isstretching exercises that you do at home.so that costs you nothing but

your time, but important for youto get better. and, you know, i also want tointerject, because the care givers that you'retalking about are all different people, so there's podiatristsand there are orthopedic surgeons that are foot and anklespecialists, and the rheumatologists are internalmedicine specialists. so you have actually sort ofmixed and matched, i believe, to many different people. which is notnecessarily a bad thing,

if they were getting somewhere. i think the mostimportant thing in any medical case -- we see a lot of this,where people are getting treated, but you really need toget an accurate diagnosis. so you have to do whatever ittakes to get the diagnosis, whether it's further diagnosticstudies, but the most important thing is listening to thepatient, hear what they're telling you, where they hurt,doing the physical exam, doing the appropriate studies andworkup to get them a diagnosis.

once you get them a cleardiagnosis, now you can set a treatment plan in place, versustreating but not really having a diagnosis. had you had any otherstudies done? i heard the one x ray, but didyou have an mri or anything else done? yes, somewhere in between thethird podiatrist/foot doctor and the rheumatoid guy, i did go into mention the hospital of special surgery in new york,which is extremely precise

when it comes to any type oforthotic surgery and things like that.and i saw one of their top fellows, and we did the --starting off with the regular x rays, cat scans, mris,so forth and so on. and now we were starting to get,you know, what the real situation and the realproblem was. so what i'm hearingis that now, for the first time, you're getting a battery ofstudies on this foot, other than just a plain x ray.

and you're doing whateverybody else here has asked you to do -- or asked them todo -- get the right diagnosis. if you're treating the wrongdiagnosis, you're not going to get better.so what did they tell you at the hospital for special surgery? heller; well, basically, because of,i assume, being born flat-footed, that the tendons onboth feet were torn, and it would require a surgery thatsounded quite extensive, where

they actually cut the bone atthe bottom of the foot, and then they take a bone frommy hip, put it into the bottom of my foot, and then i guess thetendon would reattach itself or whatever.well, the procedure for each foot is about eight months. well, the procedure isn't,right, it's the recovery? well, the recovery is abouteight months, so we're talking, you know, over a year and a halfof my life to be, you know, dedicated to these feet.so, at that point, i said,

"uh, maybe not."he recommended to wear these small braces and try them out tosee if they would ease pain. they're not going to correct theproblem, but they may make it more bearable for you tofunction, to walk around. i want to stop youright here, because now we've described an operativeprocedure. this is the first timesomebody's saying, "i've done all the studies, i've got adiagnosis, and i'm going to fix you with surgery."does this surgery sound

rational? well, i have totell you, you have me, like, off balance here,because you started out with forefoot pain.okay, forefoot pain, pain in the ball of your foot.then you said, "now i have heel pain."i don't know if it was first few steps in the morning pain, thatkilled you when you got out of bed, like plantar fasciitis is,but now you're moving into, "i got posterior tibialtendinitis," which is the tendon

on the inside aspect of yourfoot, that allows you to -- when it ruptures or elongates,falls in. so then you got three differentthings going on. i cheated -- i read a littlebit of your story. i know you got a second opinionfrom another orthopedic surgeon, who also recommended surgery. and then, on the verge ofdoing the surgery, somebody said, "don't."someone said to you, "you know, maybe at your age, eight monthsper foot, not such a great

idea."and you decided to forgo the surgery, and you wound up --you're wearing braces now. can you show us the bracesthat you're wearing? yeah, they're a strap-on.they go under the foot. i basically have to wearthese -- actually, i wear them all the time.they're doing nothing to correct the problem, they're just makingit less pain. they're supporting you. so, to me, it's giving mesome support down there, and

therefore taking awaydiscomfort. so let me summarizewhere we are, if i may. you had an injury.then you went to -- i'm counting here -- three podiatrists,two orthopedic surgeons. you've had a lot of orthotics,massage, electrotherapy, acupuncture, cortisone,lots of other treatments, and you're still in pain.this has been quite a story. so i want to be sure we'vesort of summed up where we are. a thorough evaluation todetermine the cause of foot pain

is necessary if you're going toget successful treatment. when it comes to the treatmentof foot pain, one size does not fit all.and the cause is everything. if you're treating the wrongcause, it's not going to get better.fair enough? correct.all right, so we need to move on.of course, dave is here with us today.you've had foot pain now for many years.no treatment so far has beenable

to make your pain really goaway. is it fair to say that somepeople simply have to put up with foot pain?is dave going to have to put up with foot pain for the restof his life, is that it? well, i think you've nowtrialed him. you've put him in braces, and hesays, "i'm better in the braces." right? so he is better.so now he's better in the braces, so you've -- yourhypothesis is that it was

a tendon problem.and he seems to be supported with that tendon problem.and that's -- and now he has to decide, "am i going to live inthese braces? is there another type of braceoption or orthotic option for me to sort of step down into?or should i have surgery for this problem?"that's really where he is in the decision mode. right. i want to come backto your problem. now, lisa, shoes.can you show us the shoes you're

wearing today, please? i guess so. thank you.they have heels. very high heels.are these good shoes to wear all day, every day? i would tell you that nomatter what you say, it's like, "could you stop wearing those?"well, some people feel good in those.and it's about how you feel. so i believe that we're going tohave people wear high heels.

so we're going to have todeal with it. what you want to do is have themwear them occasionally, not their everyday shoes,just to events, just when they look goodon sitting on a chair. because she's not weight-bearingon her foot with those high heels.she just looks great. i'll ask theprovocative question -- you wear these all day, don't you? all day, every day.

i'll add to that -- alot of foot symptoms are caused by a tight achilles tendon,or the tendon on the back of your leg, so a lot of peopleget foot pain because of that. so a little bit of heel liftwill take force off your foot, such as your plantar fascia,your midfoot. so a little bit of a heelhelps a lot of people. now, let me just rattle offvery quickly, now, a couple of things.crocs -- you like them? baumhauer;

i think if they feel good onyour foot, it's fine with me. earth shoes? birkenstocks? earth shoes have a negativeheel on them, which means the heel is lower than the forefoot,so for most patients, that's not a good shoe for them.for some patients who have a lot of motion in their ankle,that shoe works for them. pedicures -- good or bad? i think pedicures, you've gotto make sure you have a place that is clean and sterilizes --or at least cleans -- their

equipment.so you have to be a little careful with that. and i just want todovetail on something that judy said about crocs, or even if youtalk about flip-flops or other shoes like that.it's important that you don't have pain, because what a lot ofpeople do is grip with their toes to keep the shoeon their foot, and then they start developing foot pain. i want to get onerecommendation, maybe, one

sentence from this whole group,the best thing you can do to keep your feet healthy. i think the one thing isa good shoe. and everybody's footstructures differently. different people like differenttypes of shoes. but a good, supportive shoe,a shoe that doesn't cause you pain, is the best shoe for you. a good shoe, don't smoke,watch your weight, i mean, all these things loadonto your foot.

i just want to commenton that -- that's really important.we hear this on almost every broadcast.don't smoke -- bad vascular disease causes bad foot disease.don't get too heavy -- not only does it put pressure on yourfeet, but it can lead to uncontrollable diabeticproblems, foot ulcers, sepsis, losing your foot.bad. okay. and even if you walk 20 to 30minutes a day, that's good activity for your feet.

excellent. let's stop for a moment andwe'll sum up where we've been, then we will go forward a littlebit after that, but this is a complicated subject.that being said, there is a lot you can do to keep your feethealthy and pain-free, such as wearinggood shoes appropriate for the season, lisa.not sharing the pedicure tools -- they've got to beclean. finally, listen to your feet.they do talk to you.

you should consult aprofessional when unresolved pain or other problems impactyour ability to walk and to perform your everydayactivities. you know, dave, i understandthat people who know you say that you're always up.your spirits are high, and they would never know that you havefoot pain. how do you get through the daylike that? well, one of the things i'verealized about pain is that your body and your mind work verywell together when it comes to

something thatdoesn't feel good. i had just had rotator-cuffsurgery, i had fallen off an extension ladder, i have anindirect hernia, i have an enlarged prostate, ihave about five or six things going on.so, you know, the feet are important, 'cause they get mefrom point "a" to point "b," but they're not my whole life. all right, well, iwant to thank you very much for being here, braces and all.

braces and all. unfortunately, we're out oftime, and i hope that you'll continue the conversationon our web site. there, you will find the entirevideo of this show, as well as the transcript and linksto the resources that we can provide.the address is secondopinion-tv.org.again, thank you for watching. thank all of you for being here.i'm dr. peter salgo. i'll see you next timefor another "second opinion."

"second opinion" is producedin association with the university of rochester medical center, rochester, new york.