 Good morning. We're going to get going. Today it's my really distinct pleasure to introduce to you Anott Kessler. Anott is a colleague and a good friend of mine who is the head of neuroophthalmology at the Tel Aviv Medical Center and she's a professor of neurology and works in the ophthalmology department at the Tel Aviv University. Anott has published over 100 articles and a lot of them have to do with pseudotumorceribri which is one of her passions and areas of study. Anott is one of the people who put into the literature the different types of obesity and I know she's going to be covering that today in her lecture. And so we're very pleased to have Anott Kessler, Dr. Kessler with us today and so I'm going to turn it over to her and she's going to be talking about pseudotumorceribri and the idiopathic and acrenial hypertension form of that disorder. Anott. Good morning everyone. Thank you for inviting me to be here. First of all I want to congratulate you today is the Erebor Shachanai the Israeli epinewhears. So epinewhears and healthy for everyone. It's a very important day. Okay to the work. This is Tel Aviv Medical Center. You hear me? Okay. This is Tel Aviv Medical Center. Very nice place. You are all invited. I like to start with the case unusual one. 20 years old woman past history she is healthy. She was hospitalized due to three weeks of severe headache and transient visual obscuration. From the last three days she had also horizontal diplopia. When we examined her visual acuity was quite well. There was left six nerve paresis. People were equal and there was bilateral swollen disc. This is her disc. We can see both bilateral swollen with hemorrhage optic disc. And this is the visual field on the left. We can see the large blind spot with nasal field effect and on the right the... I'll use it. And large blind spot too. Okay we do a CT and just in CT we can see a empty delta sign of venous thrombosis. Normally you need to do CTV2 studies but in this case it was very enlarged venous thrombosis. We see we saw a empty delta sign so the diagnosis was venous venous thrombosis. We tried... we started her with anti-curgulant and dimox. And when we look in the emergency room of her blood count we saw that she had 643,000 platelets. So we look forward we found that she had essential thrombocytosis. Later on we found that she had mutation in the JNJ2. So this is example of serotonin secondary to venous thrombosis secondary to essential thrombocytosis. And so the tumor and I will repeat this sentence few times in the lecture is a diagnosis of exclusion. It's important to remember that senous ventrombosis closely mimic that IIH. The incidence of senous ventrombosis in the patient presenting only when signs of increased intracondyle pressure is around 10%. MRI and MIV or CTV should be modulated neuroimaging for accurate diagnosis in all these cases. Case II is a young boy that arrived to us from other hospital and he came with the diagnosis also due to Monterey. Neurological examination were normal except for bilateral papilloderma and six-men palsy. CTV was where normal. The patient underwent LP with opening pressure of 500, no cell, no glucose. Treatment with diamox was started. This is a sphundered papilloderma but really not so severe. One month later we routinely do MRI to patients who diagnosed with solitumor. We did MRI of the brain that performed subtle nonspecific signal changes that in this age the neurology say maybe it's dysplastic changes but to be accurate please return in two months at the MRI. This is the first MRI and you can see here small abnormal signal which were nonspecific. There was no enhancement so as I told you we decided to repeat. Three months later a second MRI demonstrate diffuse multifocal area of T2 signal abnormality in the right parietal temporal and occipital. Not brain biopsy at this point and we consult and decided to repeat two months later the MRI. The situation was stable. Very mild headache, very mild papilloderma and that's it. Normal neurological examination. This is the third MRI and the third MRI saw lesion in the temporal occipital right matter. I think here it's better. Here and here. Kind of diffuse lesion. So we refer to the intosterotactic brain biopsy and unfortunately the diagnosis become to be gliometous cerebrine. This is an aplastic kind of astrotitoma in very young, previously healthy old child with signs only of papilloderma, normal neurological examination and CT and we check again the CT that we did previously was normal. So we need to remember that this lesion mass mass screwing tumor and even the CSF twice was normal and the first CT was normal after reviewing also just by following we found that he had this neuroplastic disorder that can mimic IAH. So I just start with these two cases to remember that third tumor diagnosis for exclusion. You need to think about other things. So if you're patting intracanah hypertension of third tumor, cerebrine, what is it? First of all, a little bit of history. Third tumor, the name was given in 904 by noname. Then they think about benign intracanah hypertension by Follet and we know now that it's really not so benign. Most of the patient had quite good outcome but there are few cases with really severe visual loss. Corbett and Thompson in 89 gave the name idiopathic intracanah hypertension. Nowadays, few people call it idiopathic intracanah hypertension. Most of the people call it pseudotumor cerebi secondary or primary and the primary it's equal to idiopathic intracanah hypertension. So to diagnose pseudotumor, first of all the patient need to be allowed. There need to be signs of symptom of intracanah pressure. No localized sign despite a six-palsy. Very rarely in kids you can see also third of palsy and CSF show elevated pressure but no cell glucose normal protein normal. No evidence in neuroimaging of tumor mass lesion idrocephalus except often I will speak later about this very small signs of increasing intracanah pressure and of course no other cause of intracanah hypertension identified. In neurology, months ago, Friedman, Lew and Kathleen Degry published a diagnosis criteria for pseudotumor cerebi in adult and the children and the author proposed the patient can be self-dividing dose with primary or secondary pseudotumor and IAH and to primary and what they suggest that required for diagnosis is papillodema and normal neurological examination for chronic, except for coronal abnormality. Normal neuroimaging they offer to do MRI for everyone and MRV or CTV it depends on the hospital for case that they are not so typical. We offer MRI to everyone, MRV and CTV also to everyone of course MRV or CTV. It's need to be normal CSF composition and the point here the pressure we think about high pressure when you think pseudotumor the pressure need to be over 250 millimetre of water but what they suggest that in children of course in the right situation the cubitis and relaxation the pressure can be even higher so the normal to say someone here pseudotumor cerebi it's the normal pressure can be 280 millimetre. You need to remember that most of the people are sedated so I think the 280 it's more for sedated and not to base and for non sedated kids the normal it's 250. What is the presenting symptom? Of course headache the patients say this is the headache I never had severe headache and it's more than 90% of the patient. Transit visual obscuration very brief episode of blurred vision which may be uni or bilateral and classically participate when there is postural changes it's around 68% pulsating intracanial noise you forgot to ask the patient but if you ask they say oh yes I had a noise normally they came I had a headache but if you ask them correctly they say yes I had a blurred vision sometimes I had a noise like tinnitus diplopia and visual loss between 10 to 30 percent. Design papillodema even severe papillodema non predictive of visual outcome visual field it's obligatory and it's the right way to follow the patient we can see in large blind spot in for another visual field and visual field construction and of course can be also decreasing ocular motility. What regarding the demographic and epidemiology the incidence is sort of two more around one to two per hundred thousand in the general population but when we deal with childbearing women it the incidence jump to 3.5 to 4.5 although we need to remember IH occur more frequently in the adult it's occur also in the pediatric patient and we have a very big pediatric so the tumor therapy even younger than five three and two years old it's rare but it exists in 98 and 99 we check the epidemiologic of Israel of IH in Israel because Israel it's country of a lot of people from other country arrived in those years so we decided to found what is the prevalence and what is the incidence and then we found when we calculate that it was really the same as it was in the state it was around 0.57 to 0.9 per hundred in the general population and the incidence jump to 4.02 when you deal with women age 1545 nowadays we did the epidemiology in Israel in 0.507 because we had the feeling there is too many people and what we found that the average annual incidence rate was two zero two per hundred thousand and the incidence of course would jump in women and in female during childhood the incidence was five point four nine per hundred thousand our findings show an increase incidence IH in the last decade in Israel and it's almost three time higher the rate that was found previously this finding was and require an immediate national action to play in the fight the obesity epidemic to reduce weight and prevent overweight among of course all age group obesity as all of you know is the most common finding in IH over 90% of the women are obese it's not that someone tell her that she is obese they are really obese the BMI is over 30 35 or even more it is known that maltress and weight gain was highly correlated with poor visual outcome in this patient and they increased degree of obesity were associated with increased risk of severe visual loss so obesity play again the rule of obesity in the pathogenesis of IH is suggested by increased incidence IH which parallel to obesity epidemic all of the world one hypothesis is that the visual obesity cause elevated intra-adominal pressure is something in increased central venous pressure and leading to increased intracanial pressure so obesity usually classified by BMI body mass index but this measure failed to address the increasing important feature of the original distribution of adipose tissue and specific fed distribution is often determined by measure the waist to hip ratio which is that circumference of the waist divided by the circumference of the hip so we speak about apple and pear nearly all the systemic complication for obesity such as hypertension diabetic have been linked to visual a deposit it's central or abdominal presumably due to unfavorable metabolic feature of the fat cell comprising the visual in contrast genicoid obesity or low body obesity characterized by subcutaneous fat deposition in the lower body including the gluten depot and low extremity appear not to be linked to cardio vascular complication so we decided to characterize the obesity penalty in IH patient we took 44 consecutive patient in our clinic the diagonals with IH according to what if identity criteria and we use to control group to reference group one we took from the first Israeli national heirs and nutrition survey conducted by Israeli ministerial in 1990 and the other control group was consequently referred or best woman from the Tel Aviv so asking medical center obesity clinic and this is just example which the hip circumference that was higher than the national serve in this IH patient but less than the basically the waist that was lower in the IH patient and if you calculate the waist to be pressure it was lower in the IH group wasting weight circumference of IH was smaller than the control consequently WHR was significantly higher in control compared to the IH patient so this show us that it shift to the left compared with the reference group so it's consistent with what we call preferational deposit of faith in the lower body lower body a deposit II WHR less than 0.76 was seen in 45% of IH compared to only in the national survey of 2.1 and in the obesity clinic of 77 this graph show you are you divided the lower body or deposit it's less than 0.76 and upper body a deposit if it's over 0.85 and this graph you can see this so this is the obesity clinic the national survey and the IH group that clearly shifted to the left compare with the two reference group so now we decided okay you can see it's not common but you can see so the two more so in men so we want to know what is the obesity pattern in IH in men because it's around 10% of the patient with so the two more are men so we had 22 male with IH we compare them we control control group that they are came from the health program in Tel Aviv Medical Center with match for age and BMI and also compared to our previously group for the female as just I mentioned this is the central obesity WHR in men it's over 0.9 in female 0.85 and genicoid or lower body a deposit less than 0.76 and it was very interesting because the man was less lower body a deposit compared to the woman for the sick woman the men and the woman with IH if we compare the men with IH to the healthy men the men with IH as more lower body a deposit so what we can see that the central obesity in the healthy men it was 65% in the male with IH it was 45% in the female right of course it was very less so we conclude that is that the men with IH is less central obesity compare with healthy men but more central obesity compare with women and we still think that IH mailing to more genicoid pattern so we say okay we need to continue because if our observation is right that IH is associated with lower body a deposit we wonder whether or not the presentation of IH percent or the fat distribution IH might be linked to any unique hormonal profile so we took the female but we had and we check the hormonal profile of course we cannot check all the hormonal profile but we check few of them and what we found that there was no difference we don't find high extra the old for example we expect if you have lower body a deposit that this patient will have higher study all because it's called a genicoid no but the only thing we found that IH at an age younger than 25 years at the higher level of testosterone beta testosterone and under the testosterone and they do accept the testosterone increased level of circulating and again are searched with early onset of IH and this finding is particularly interesting since most common well-defined form of overt hyperanandroganism in the best one is polycystic ovary and we know it's very common to find polycystic ovary but polycystic ovary with some time we linked to the abdominal obesity so it's raising the possibility of causal involvement of hormones such as androgyne in the pathogenesis of IH the link of IH to androgyne may also be expert or even underlight the better recognized association of IH with drug using the treatment of female for example tetracycline or a cutan this finding comprised sufficient as we thought justification for further reassessment of the rule of androgyne in female with IH patient neuroimaging it's obligatory to do neuroimaging before you say the patient had IH also the two more my broski 98 the terminal very slight side but I think very important of sign that we can see in MR of patient diagnosed IH so all these signs it's signs that help us to think maybe that this patient and IH because the result of the neuro-ageology is normal brain imaging but if you look carefully you can see enhancement of the perilaminar optic nerve you can see flattening of the posteriose like sclera you can see empty cellar so for us and it's important that we look by our self after the know a georgia death of course is result and we look for this small sign when you think maybe this patient and IH and based on the MRI sign the examiner can able to predict the presence of elevated intracanopathy more than 90% this is example for city axial city it's normal you can see the optic lobe and here you see the reverse optic nerve and it's like you'll see the papillodermine neuro radiology another example you see into weighted imagery fast pin echo axial imagery with fat suppression you can see anterior protrusion of the swelling of disease with this tent periopula peri optic CSF and it's very common we look at this and we see all there is a large optic nerve a lot of fluid it's help for us to diagnose we decided to establish what is the because we have quite a large go for so the two more terrible in kids we want to know what is the normal optic nerve diameter and if it's really correlate with increasing the optic nerve diameter with a patient with IH so we decided to do it with kids we took a kids not the kids that picture of the kids and we measured one sentiment to the optic for Amina in axial T2 sequence and we divided the patient to four group 0 to years 3 to 6 year 6 to 12 and 12 to 18 and what we found that the main optic nerve sheet diameter in the normal was a little bit higher with the age but it was around 3 that we know this is the normal optic nerve sheet diameter and in all the patient with IH there was increase in the diameter of the optic nerve sheet and this is just example the way we measure it the optic measure was 10 millimeter and tell you to the optic for amen and in this example you can see the distance in green of the optic nerve and if you could compare it we can see that there was a large optomethia diameter in kids with so the measure of the optic nerve is we think is an actual tool in the diagnosis of increasing the pressure in pediatric patient we think also in the adult but we didn't do it in the adult group little information is available regarding psychology impact and quality of life with individual with IH clenchment in and Catherine the green in sorry was the first to look and to explore the incidence of depression and exciting a life in IH they checked 28 women with IH and compare them through 30 control group and what they found that IH patient were more depressed and unexciting the normal weight control and there is link obesity and psychology difficulty but obesity alone doesn't explain the depression and lower level quality of life we are now collected our data of patient with IH we decided to examine their cognitive function and the purpose of study was to evaluate this cognitive function using I don't know if you know you know this technique neural neural trackstays this is a practical and technology advanced tool which provide both fulfill of cognitive function have been show precise and easy use with good with this ability and discriminate validity for mild cognitive impairment it's a computer test the patient sit around 30 minutes this is just I don't want to enter into this example of the modality of the Neurotex and for example this is example for the nonverbal memory the patient need no they showed they after four five minutes explain the patient and to be sure he has understand and repeat then we start to show him this picture a few time any to remember for example if this it's straight or it's down to the right on the left and this is another example of executive memory that he says large color stimuli are present at pseudo random interval and the participant instructed to respond as quickly as possible by pushing to the mouse bottom if the color stimuli is any except red and it was interesting how we found the results we have 30 consecutive patient just consecutive patient that arrived to a clinic and they agreed to participate and it was very interesting when we told I told him you know I want to find if you have any problem cognitive or we have any problem in memory say oh thank that you asked me no one asked me this question because you know we do with optic nerve disease and what we found that there was significant difference from the average domain except for memory which was short trend toward abnormality without statistical differing that there is decreasing a lot of cognitive function and our results found that there was mild cognitive impairment using this computer test all the main measure apart from memory show the statistical significant different from normal individual consistent with mild cognitive impairment indicated there is a form of multi domain cognitive impairment in it you need to remember they had high pressure in the brain so it's important we start with this we need to continue but I think we need to ask the patient and to be and and to understand that they had another problem despite the problem that they are very important of course of preserve their visual function condition of associate condition of to the tumor associate they are it's not all the list and if you see so big list it means that you don't know I just want to mention one point of vitamin A because it was presumed by Judy Werner that high level of so the patient with high H at high level so but lower level of CSF retinol binding protein you need to remember most of the people the woman had had and they use a lot of material with a lot of vitamin A and she suggests that the present of unbought toxic retinol that might interfere with the pressure regulation provide evidence that the vitamin A may be involved in the petrogonase of high H and for and we know that we ask the patient with me we take an amnesia from him which medication is taking and we vitamin A especially with high vitamin A for us it's a sign maybe it's one of the cause of this so the tumor in this patient but surprisingly in the last two years we had four or five children that had low vitamin A and and we found it it was associated with so the two more two of them were autism that died they just eat the schnitzel I don't know I think it's schnitzel it's international right now they just this it is and we found very low level of vitamin A and we now check the level of vitamin A in every patient who under 15 years old that entered to our department to see and we were surprised there is a lot of vitamin deficiency in this it's not so simple because it's depend on the way you check the vitamin A but we think hypervitamin of this a it's not good but hypo it's not good the pathophysiological mechanism of high H has been source of controversy and it all the towering needs to be explained several features first of all the predilection for obese childbearing woman lack of ventral megalene and identical clinical feature from other etiology side such as sinus ventrombosis so there is a lot of etiology we think about increases of production in your CSF absorption associate medical disorder intercontinental potential so multiple toria but no and unifying hypothesis one of all the regarding increased CSF production we don't think according to the literature that there is increases production but the first drug we use is carbonic anhydrous inhibitor this carbonic anhydrous presenting the horid plexus and catalyze the formation of carbonic acid from water and carbonic dioxide and play an important role in the sequestration of horid fluid it is found that inhibition of the enzyme resulting in inhibition of formation of CSF also treat with IH at center around decreased CSF production because we use that set as a limit the hypothesis of a production has never been supported by experimental data and over production of CSF seems seems unlikely cause of this and the Korean metabolic dysfunction for sure there is a connection but we don't know yet there is a lot of work we need to do regarding the adipose because we know there's different between when we speak spoke about central of the positive between the type of the adipose the central and the type of the adipose in the lower body you cannot speak about so much there without speaking about the intracanel venous hypertension I just mentioned the king that was the first in 95 and then in ZOT this is a group from Australia I think that the only one who can get IRB to do this so they did that cerebral venography and manometer in nine patient with IH and the venography show narrowing of the transverse signals and they found that reducing the venous compression reduce the CSF pressure a fab in neurology zero three make a nice diagram of the type of the stenosis and they also used mv to show that in 90 percent of highage patient there is stenosis in the transverse signals and nowadays we know that transverse stenosis it's very very common in every patient with IH but we can see it also in patient without IH and one hypothesis of that the hypothesis that there may be there is a primary abnormality in IH such congenital narrowing of the transverse signals and presented of that very appeared later because of things that we don't know yet the the clinical began to present maybe underlying venous sinus abnormality create flow limiting stenosis and resultant impressive good yet and the clinical become reach we gel in neurology zero three the clinic found the clinical course of IH was with transverse stenosis is common as I just mentioned there they don't find any correlation between the decree of the transit synosis and the clinical course including visual feed loss among pension IH suggesting that the clinical feature not a degree of the transverse stenosis should be used to determine the management of IH and I think it's a very important point as I mentioned just synosis transverse the stenotic transverse signals is very common whether it's the cause of the consequence we really don't know yet we are we still presume that it may lead to impaired venous outflow without to reduce pressure in the arachnoid granulation in the acid in reduced CSEF absorption but it's not enough data for us today so still the answer the chicken of the egg the cause of IH a lot of words but still mystery and we need to continue to look for it I think the most important thing is to treat and to know how to treat the two goals of the treatment are first of all reserve vision and I live symptom of IH particular header because if you had so severe headache you cannot do anything and optic nerve function should be carefully monitored it's include visual field that I think it's very important parameter and the appearance of the fundus regarding OCT that I know in the terminology ever patient entered the clinical first of all do OCT in Israel I don't know how it's here and it's not enough it's good for follow the patient to see if there is decrease in nerve failure but I think till now the way to follow it's it's visual field it's very important of course to compare all the parameters so we want that the patient we lost his weight it's easy to say it's very hard to do they are very fat and they cannot they try but it's take time and it's not first line we speak with them we add in our clinic psychology clinic psychology they help them but you know they are very very I said as all of me the carbonic anhydrousinibitol that is the first drug you need to remember that this drug had a lot of side effect it's not you need to explain the patient if you explain the patient you can take the medication that parastasia that metallic test and they can possess stone in the kidney and very rarely but it's happen a plastic anemia now in here in the state the NIH proceed multi-center trial comparing efficacy of acetazolamide and placebo in treatment of fire age with moderate visual field effect all patient also treated with low sodium diet and participate in the weight loss program and we will rate the result of this result because till today acetazolamide is that it's not it's what you call a on over the counter medication for topi topiomide anti epileptic drug is also carbonic anhydrousinibitol but less severe you need to remember that it can cause myopia and glaucoma so especially in the beginning with we check the pressure to this patient and we see a few patients that start open armad and came all I had to decrease in my vision and the crystal vision was because of eye intraocular pressure and not because if I intra cranial pressure steroid brief course of eyes those steroid may be useful when there is the duration of visual loss but long term steroid are not routinely we are not doing it first of all because of weight gain fluid retention and there is also debate regarding the withdrawal of steroid surgery surgery is required for fulminant onset or when the treatment it's not enough you do maximal treatment but there still deterioration in vision you have today three option optic nurse finish optic nurse administration diversion procedure like LP shunt or VP shunt it depends on the neurosurgeon and standing of the transversinos optic nurse administration it's very elegant it's help when there is problem with vision but where there is after and popularity thing you're afraid there's a lot of field around the optic nerve that compress him and you're afraid the patient will lose his vision but if you have had it wouldn't help and for this you need to do shunting so a lot of cases we do medical maximum medical treatment there is deterioration or after and popularity effect we do a opting nurse if it doesn't help we do the shunting procedure the shunting procedure they help but there's a lot a lot of side effect there is a inflammation there is stenosis of the shunt and sometimes there is over drainage and you need to remember and over drainage can cause severe headache standing of the transverse venous stenosis it's now in a few places they are doing it it's endovascular venous standing it can result in serious complication you need to remember it the stent can migration can be subdural hematoma develop of recurrence stenosis nowadays it's there's no enough prospective control data so and the result of efficacy today are inclusive so it's not a routine only for a special case may can be we need to still wait for the study that we are doing I know in the state to see the efficacy of this treatment regarding the outcome the unnatural history of IH is unknown and some most of the people we know it's self-limited disease but in few people there remain I increased the pressure remain very high for years and visual symptoms can resolve but some patient and a lot of recurrence but in most of the case there is a self-limited disease after around six years and we check it and we found that the most common recurrence are in the first six year after six year it's very unusual but can be and we off we all the time offer the patient after this period of time just to be followed it's one point that I want to mention it's complication of IH that I think not most most of the people don't think about because they think IH at Papilla Dema lost a vision but we in the last years we found four cases of spontaneous cerebral vascular otter and rhino rare due to IH one case was 45 years of female obesity with some typical Pella Dema she had no with IH in zero she was stable visual function and visual field and she was really non-compliant for treatment and then she arrived because she said I had a headache but the main she had a pain in my ear tinnitus and autophonia EMT examination of your material bearer was normal we repeat the MRI and CTV no senous ventral boses but she say I had a autophonia and we repeat the EMT examination and we found pulsatory treatment on the tympanic membrane with air in there her middle here and was suspect of FCSF otorea and this is imaging we can see the FCSF the other case was 48 female with she was obesity all the cases with rhino rare was really severe and she came because she had headache but not so severe and Papilla Dema and a few doctors say maybe it's not Papilla Dema maybe maybe it's sort of Papilla Dema and she came to us and when we asked her a question she said yes I had a fully fluid discharge from my left nostril but it's nothing for its last for the last two months we do LP we examine her fluid we the fluid was collected for the nostril to found a positive for better to transfer it better to transfer in producing the horrid plexus and it's only found in CSF and when we do imaging for air we can see and cephalo cell entering from the creepy foam plate to the etymoid bone so it's extremely rare complication but may become life-threatening if left untreated so we need to ask the patient if they are tinnitus if they're dipping from his nose from their nose I H in pregnancy you know a lot of I'm called a lot of call I had a pregnant woman what to do stop the pregnancy every day and at night we have a question I H can occur at any trimester there is no increase in maternal fetal neonatal mortality visual outcome is similar to that of non pregnant patient with I H Kathleen was published in 84 a control study demos that the pregnancy is not a theological factor but still a lot of people and a lot of physician they are afraid and a lot of gene ecologists also at CETA Zolamid of course it's classified as class C according to FDA but we use it in the to treat if we need to treat there there was a case of saccharocortical teratoma in infant born to mother that was treated with CETA Zolamid but she was treated very very high dose of it throughout pregnancy so we if we need to treat the patient we treat the patient it's depend of the I the reason if there is we're afraid yet severe papilloderma visual field load we need to treat we treat and follow it carefully follow the patient carefully I H is not by itself a specific indication for Chezanne delivery labor may be a lot by the Chezanne delivery only if there is indication gene ecological the indication there is no contraindication for another pregnant there is no connection with I H who wish to become a pregnant to become a pregnant she just need to be follow up by Neurob so in conclude many question remain unanswered about I H also it's a common in a best female it's can occur in men in non-obesed adult and in children but the physiological study as well as clinical try should provide more insight to this thank you thank you for the question I agree with you you will excuse me that in the states there are few people are very very best I never seen such case in Israel but yes you can see if you sit out of the door my clinic you say oh this patient it's for sure they are really obeys and they increase you know israel it's five years later the state so the obesity epidemic can continue yes there is enough best woman most of them yes there is improvement when they lost their way yes and they there is a kind when they say oh I eat a lot at 10 15 kilogram yes I think lost but not to do a surgery because what happened with all the surgery if they want to the problem is in the head the head and with I think we need to check if that problem in behavior by eating alone because they can if they had a operation some of them after a period of time if they cannot eat meat they will eat will milkshake and and they become again so I sent very rarely only if I can't I've no success with I had in my clinic that the psychology and nutritional I keep just for the last chance but even with this operation it is with the new operation for gastric type some of them continue to bring the milkshake with the control be sure that we found we thought there's angulation no if we check we choose the same sequence and the same name there was there was no angulation because we choose that the point that there is no angulation it's straight so you can compare it with the distance of 10 minutes exactly started we check a lot of other plants of the it's wonderful question I don't have answer we just found this we don't even publish it yet because we were surprised now first of all we need to continue to check it then we need to check this patient after treatment after the age will pass and then thank you for the question I think it's it's quite obligatory that you have to fill a demo there is what we call but it's very complicated you will excuse me because if you check a patient with migraine and you can check the pressure you can see high pressure so we had no so I think it's very rarely and we see very rarely patient with normal with normal optic this and if we see the optic is normal we say maybe it's other disease because my genetic and see a lot of fine that arrived you made the question you can have a high pressure so but maybe and other things you know this is a pseudo tumor so it will be so the pseudo tumor it's too much very polite human excuse me I need to speak in English I was born in Israel and I'm afraid I made so many mistakes no it's fine no one by one because I think but then I take them and not look like but I'm very polite this is I'm grieve with you under percent no because you don't want that especially with the younger one because of the anorexia and you know that there is one patient of mine that she decided to lose the way and she become anorectic so I am I'm very careful I don't want it and I explain them I don't want it you start yourself I just want to three kilo months very very slowly if I deal with one hundred and more this is the tough cases we see it's very an orphan called full name for the tumor in the last year they are not totally blind but they see perception or six they're almost blind or construction there we added and it's very we treat them as fast as possible what we do what we did especially they arrived just with the reaction of vision so they are in my experience which unfilled and also with most of them we do often no shit demonstration immediately if there is no response after 24 hours of L. P. Shan and we treat them in between with steroids for very short period of time but we found that in this tough cases for short period of time to do so you know it's safe time for the operation