 So coming to today's session, it's my pleasure to welcome Dr. Hiren Panwala who will be taking the pediatric neuro radiology general club for us today. He'll be discussing an article on MR pattern recognition and childhood bilateral basal ganglia disorders and also a few cases following that. It's my pleasure to welcome Dr. Hiren. He is a pediatric radiologist at NHS RCC Children's Hospital in Mumbai, is areas of interest of pediatric neuro imaging and pediatric chest imaging. He's done his fellowship in pediatric radiology at CMC well Lord, and a short term observership in pediatric neuro radiology and the great Ormond Street Hospital in UK. He has published publications to his credit and also has authored several chapters in the upcoming I write this textbooks in various topics in pediatric neuro radiology and and cardiac imaging. It's a pleasure to have you with us Dr. Hiren, and over to you, you may please take over. Yeah. Thank you. Thank you for the kind introduction. Am I audible. Yes, you are. Yeah, so the screen is visible like my. Yeah, you can. Okay, so once again, thank you organizer for giving me the opportunity to speak on this topic. So today we'll be discussing on this large group of condition, which is bilateral basal anglia disorders. And this is the article which was published, published in the brain communication 2020, and it's a retrospective study, which was done across the multiple centers across the world, which which were located in Sydney, London, Birmingham, Lates, Portland and Barcelona. So they had reviewed 308 308 MRI scan, and out of 201 patients. And based on that they have categorized some 93 diagnostic categories. Here is we can see that this is the primary author Dr. Shakip, who has collaborated with other part of the country and made this beautiful article. So we'll be discussing and going through this area. So they have given this wonderful way of giving a graphical abstract that was, I was very happy to see this kind of way abstract can be sent. So they have what they have done that all the basal ganglia, they have clustered into different different categories like, for example, we put on a moment for example with global spell it is in moment, or other parts of the brain stem and other findings that will be going through this thing. And based on that, they have given us our approach. So starting with the introduction, the basal ganglia, they are the bad deep gray, white, white metal structures, and they comprise of corded and putamen, which are known as triadome. Other thing is global spell it is, which you all know, substantial nigra subthalamic nucleus and nucleus equipments. These are the high energy dependent area. So they are very vulnerable to toxic hypoxic or systemic injury, and they have predilection for many genetic and neurodegenerative disorders that will be going through. The thing is that approach to a bilateral basal ganglia is very difficult because there are a large number of disorders that can involve the basal ganglia, especially bilateral. And the most important thing to evaluate a case of basal ganglia disease is clinical profile. We have to see first that the presentation is acute, subacute or chronic, whether the disease is static, like for example, sick failure of prior insult like HIE or hypoglycemia, or it is progressive, like for example, neurodegenerative conditions like NCL or some neurodegenerative or dystrophy is like, kind of, and so on. And you should have some other clues, like the patient presented with encephalitis or rheumatic disorder like X-apiramidus symptoms or cerebral assign. So this kind of detailed history is very important, approaching to a list of differential diagnosis. Then, when we have taken this clinical context, imaging pattern, which will help us in narrowing further down the differences, that will be seen in subsequent slides, how we can further down the differences. And based on that, we can give or suggest targeted investigation in certain disorder, so that we can save a cost also, and we can directly point out that this abnormality can be seen in certain metabolic pathways and we can do the test regarding or limited to those areas. So this was the multi-center study which brings up the large cohort of patients and they have formulated a diagnostic algorithm, how to go about, and they have made a prototypic electronic decision making tools. So we can preview these things later and at the end of this session, they have made one nice software that we can access through the online platforms and we can try to solve our case also. So, first of all, we would like to revisit the anatomy. So basically mainly they are made up of this thing, Globus Pelagus and Corpus Tritum. So we can see that Globus Pelagus, generally they are slightly more hypo intense as compared to the corded nucleus and the putamen. This is the corded nucleus and that is the putamen which is lenticulant shape and the middle aspect of these two pairs structures are the Globus Pelagus, which are slightly more hypo intense as compared to the corded nucleus and putamen. Here this yellow color structure is the putamen and this red color structure out in the area is the corded nucleus. So the corded and putamen they are almost iso intense with the gray metals. So that's the way we can say whether it's they are abnormal or normal. And the Globus Pelagus will be slightly hypo intense. So that is about the anatomy of the basal ring here. There are a few other structures which comes under that basal ganglion circuit. One of them is the subthalamic nucleus. So that's how they look nucleus. They are also a bad structure, which is medial to the corticospinal disc. So you can see that this is the long and slightly hypo intense white metal track that is the corticospinal track. So this subthalamic nucleus they are located medial to this and they will be ventral to the thalamus in this location. Then another thing is the nucleus accubus. So the nuclear accubus is very difficult to see on MRI. But here we can see that they are also a bad structure and it is coming enter or infer to the corpus tritum. So that is the one number one label. It's the corded nucleus. The second one is the putamen. And here we can see that the entire infir aspect of the corpus tritum. That is the location of the nucleus accubus, which will be seen in relation to the anterior commission as seen on the interview. Yeah. So coming to this article, the material and methods. So they have included all the children ranging from zero to 18 years having bilateral basal anglia abnormalities either on 1.5 or three dash limeric. Their excellent criteria were that they have excluded some conditions like disorders of neuronal migration, migration or neuromelastic conditions like basal anglia or germinoma or neurofibromytosis. They also have excluded any cerebrovascular insult related to basal anglia injury, as well as unilateral basal anglia. So all the cases they have selected, they were having bilateral basal anglia abnormality. They also defined the disease categories as per the latest journal and peer reviewed articles. And these are the some examples of these conditions like ADEM, NAC, basal anglia encephalitis, which can be autoimmune. So that you can go ahead, this is available online in a supplementary table two with this article, and you can use this definition for the particular disease. They also had done cohort of this 201 patient as well as done a peer reviewed publications to incorporate certain other conditions which were not included in this study to widen the scope of all the clusters and which can be comprehensive in nature. So the patient data which they were mainly taken as a children's hospital where it's met in Sydney, as well as Great Ormond Street Hospital in UK. And it was a retrospective study. They also developed an MRI writing and performer. So you can see that this is the claims of the performer how they have evaluated each patients on MRI. And you can see that they have individually labeled each structure here, chorded putamen, global spellidae, substantia nigra, subthalamic nucleus, and depending on various signal intensity on different sequences, they have made this kind of columns. So they have included multiple categories, whether on day two they are hyper, hypo, they are symmetrical or asymmetrical, different there is restriction or not. They are having susceptibility or low signal intensity on SWR or T2 star technique. This is the appearance on T1 weighted images. And is there any enhancement on post-catering? So these are the parameters they had used for each case. They also had evaluated excess tidal changes, those patients who had business lack of normality. They evaluated other part of the brain also, like for example gray matters of the superficial structures, white matter, whether white matter was in only Periw and Trippler, deep white matter or was there any specific locations of abnormality. They also included, is there any midline structure enrollment or cerebellum brain stem enrollment. They have also incorporated the other findings like how is the myelination pattern, whether it's hypomyelination, delayed myelination, and whether the hypothalamus is normal or not. So it was a very comprehensive review and this many parameters were used. And so they have included 23 MRI features which was based on the MRI abnormality as well as type of the MRI abnormality. So for example, the signal intensity that we have already discussed. And based on that, they have done cluster analysis, which was based on this agnomerative hierarchal clustering analysis using our software. And based on that, they came up with this kind of basic abnormality which can be grossly scattered in this kind of full time kind of cluster in which this orange color cluster represent cluster one, which indicates this patient had predominant T2 weighted hyper intensity or strident like audit nucleus also. Then the cluster B is this kind of light green color in which we can see that in this cohort or in this cluster, they have included those patients who had either T2 weighted hyper intensity in global pallidus or who had SWI blooming or susceptibility. So that was the cluster two. In cluster three, they have included those reason who had global pallidus enrollment, plus those who are having T2 hyper intensity as well as in addition, those who had receptor diffusion. So there was quite overlap between these two conditions, the cluster two and cluster three that we can see on the figure all itself. And the cluster four was more isolated and it was showing that T1 weighted hyper intensity on this ring without any restricted different or susceptibility. So they came up with this kind of four kind of categories. So total 305 range can be developed. And in this study, they identified 34 diagnostic category, but they reviewed and then the diagnostic category were increased by the review of literature from other journals and all. And that diagnostic category increased up to 93. So that's a large data. And out of this 201 patient, 84 had two or more sequential scan also available. So they have done a follow up of those patients also in which they were finding the follow up scans. There was some findings like certain disease, for example, mitochondrial current science syndrome, and so on, they have overlapping features like for example, they would have initially presented as a cluster one disease, but then on follow up scan they would have shown additional hyper intensity in global pallidus and so on. So they had this kind of overlapping features in these conditions. That will be seen in the subsequent this article. So this is the table which is showing that the claims of the entire study that they have included this kind of 34 diagnostic group, which included this kind of metabolic disorder to neurodegenerative disorders to some sort of HIE, then inflammatory conditions like ADM, and so it was a large group, and they tried to sort it out by cluster. So first of all, we'll start with the cluster one that is the bilateral butaminal or striatel hyper intensity. So that was a major group in the study and 91 patient out of 201 patient had this kind of butaminal or striatel hyper intensity, and they came up with 15 categories in this study, out of which the majority of were them ADM, and then followed by the clutteric acetylene. We'll be seeing now interesting cases in this cluster only, and their particular features and what are the clinical findings and the teaching point within these clusters only. So we'll start with the first case that is the clutteric acetylene type one. So the clutteric acetylene type one, the classical presentation that the child might have microcafely. They have encephalopathy crisis just after a follow it by a trivial trauma or fever or an infection. And if you do MRI, this child will have this kind of classical abnormality in the form of you will see a few swelling of the bilateral basal ganglia predominately the chorded and put on it that is a striatel. They can evolve the global spell it is also other thing that this child may have this kind of subtle if you run so subtle hemorrhage, which is shown by this kind of green dash arrow, and they will have this classical under operation of the temporal poles that we can see anterior here because, and they will that will lead to this kind of widening of this even future, and that gives rise to appearance of the battery. So when you see this kind of history, and this classical imaging finding, you can straight away give a possibility of possibility of this kind of the type one. The other differential for this kind of subtle hemorrhage would be a non accidental injury, but non accidental will not have this kind of common and correct. So that in that way we can differentiate those kind of differential disorders from the type one. Moving on to the second entity, when you see this kind of involvement of the basal ganglia symmetrical chorded nucleus and put them in with. If you see here there is pairing of the peri ventricular and deep bite matter in the bilateral cerebral hemisphere, and there is involvement of the sub cortical white matter. You can see they are symmetric and there is some gradient so the anteriorly in the frontal lobe the findings are more consecutive us and as compared to the posterior aspect. And here we can see that there is some involvement of the dented nucleus also. So this condition is called L2 hydroxyglutaric aciduria. So when you see this kind of combination with the sparing of the thalamide and classical involvement of this kind of dented nucleus, which is seen in almost all cases of this patient, then you can raise this possibility of possibility of L2 hydroxyglutaric aciduria. So the teaching point here would be that imaging features are characteristic and this isn't sometimes they can be dispersed to brain divorce so it's important to follow these patients. So this is the case of L2 hydroxyglutaric aciduria. So the another type of metabolic abnormality which can affect the basolidia with hyper intensity of the striatum and butamin is propionic acid. So the propionic acid they have to kind of form either they can present early in life or later in later in older childhood age group. The early presentation in the new age group they present with hypotonia, lethargy, caesare and coriathere movements. The classical clue would be that in some many of the patients they have this kind of ventrolateral or central linear hyper intensity thalamide. This is not in all cases but in this cohort in this study they have found that many patient had this kind of abnormality in the ventrolateral or central part. So the thing is that if you don't see that doesn't exclude propionic acidemia but if it is seen then that will be a clue towards this condition. They can have dented nucleus hyper intensity also as you can see in this image. So they have observed that in older children in the basolidia in older children the basolidia was more commonly involved as compared to the near-age group. In near-age group there is another different kind of MRA imaging finding you can see that will be in moment of the cortical and subart cortical white matter which can so restricted if you run in the acute phase. So these are the hallmark features of the propionic acidemia. And moving on to the there are some lesions which will be almost near CSF signal intensity as we can see here and they are almost cavity or vacuolating lesions which are symmetrical. So when you see this kind of symmetrical cavity or vacuolating lesion which has almost CSF signal intensity which is involving the corded and putamen with relative sparing optic lobe spelliness. And in this patient we can see there is evidence of cerebellar atrophy as evident by this kind of interpholar space winding as well. And you can see that this is the MRS which is run on low T35. That's why we are seeing large lipid lactate peak here. If you do 140-40 you can see that inversion of this peak. So that's a lactate peak. And this condition is known as leak disease. So this disease can be caused by multiple mitochondrial complex gene deficiency. Here the clinical history that the patient might be having subacute necronizing encephalopathy. And the lesions are spongiform and you can the patient present with granuloplastia and aphthalogea. So here the clue would be symmetrical areas of necrosis or cystic changes. Another thing I want to convey here that many patients will have striatal atrophy on follow-up scans. So initially it was thought that this striatal atrophy is because of post-triptococcal infection or it happens only in mitochondrial disease. It's not the case. So striatal atrophy has many diseases which can follow it. Like this is a long list of differentials which can cause striatal atrophy. So it starts with a finding. So we should stop writing when we see striatal atrophy only a few disorders. There's a long list. Then we're going to another disease which can be diagnosed on MRI is this condition. So the child presents with macrocephaly and neuro regression and water delay. And if you see that what is the classical finding in this child is that symmetrical areas of white matter hyper intensity, which is having more predominant in the frontal lobe as compared to the paratoxibid region. And you can see that there is hyper intensity and almost swelling and cystic looking areas of the chronic nucleus as well as some portion of the butamen as well. Another classical finding you will see in this kind of patient is that this kind of post contrast enhancement along the ventricular margin. It's almost look like garlic. And the same area will be seen as a as a T2 hypointance band along the periventricular area. So when you see this kind of combination of finding in an infant with this kind of history, you can raise a possibility of Alexander disease. So the teaching point here is that garlic sign and Alexander's disease also can have optic asthma technique. Optic asthma technique can be seen at the disorder so that will be seen later. Then in this group, in this condition they have found in this article that there was a certain disorder which which had ream surrounding the butamen. So these are the examples which can have ream surrounding the butamen in this article. So one is the myelinalysis. So myelinalysis happens when there is this rapid correction of the sodium or it can be seen certain conditions like metrological malignancy or SLE or diabetismalitis. Or any other electrolyte imbalance can cause this kind of myelinalysis. So you will see this kind of peripheral hyper intensity and spelling of the putamen. As we can see here, they can also involve the thalamus and the dorsal brain cell. So that is these are the typical imaging features of the myelinalysis. That is relative sparing of the ventral thalamus that is that we have to see observe. So when you see this kind of imaging finding with this kind of history, we can make that this could be due to myelinalysis. And the MRI changes, they are reversible, but they take weeks, two months to resolve on MRI. Then another very severe formative condition which can have this kind of appearance. This is the formative encephalopathy which can affect the infant and children. And it can be caused by various viral infection like influenza, rotavirus, HSV. And now in the current scenario, COVID also can produce this kind of lesions. So these are the multiple bilateral, near-symmetrical necrotic lesions in the Beja Gangla and as well as in the thalamine. So thalamine bilateral symmetricity is the hallmark of this area which involvement of this putamen and caudate nucleus. They can show this kind of trial laminar pattern of the ADC in which the central area will show us necrosis or hemorrhage. And that will be high signal intensity on ADC surrounded by this kind of risk. This is a different low ADC value which indicates cytoxic edema. And peripheral this kind of again facilitated difference which is showing the vasogenic edema. So when you see a child with this kind of active disabilities and permanent course and when you see this kind of imaging pattern, you can see that this is most likely to be a neck and they can start steroid and save the child. So thalamine coverage punctured their classical hallmark and this kind of trial laminar pattern seen on ADC map, you should look for that and that could be giving away. And sometimes this NA can be secondary to genetic conditions like RnBB2 mutation also that we have to take into consideration. Then sometimes uromia also can have similar kind of pattern with swelling of the corpus triadome with relative sparing of the globus pelletacens surrounding the putamen. Otterminensia pelletis, yes it is a disorder that we are not able to prove it even though doing multiple laboratory examination. But this patient usually the swelling is homogeneous and hyper intensity is also homogeneous as compared to the patchy distribution which is seen in ADM or other conditions. When if you don't need this patient, they can go into progressive atrophy of the building as we can see this is the fall off scan of the same patient. And the usual antibody which is diagnosed is antidote part 2 receptor antibody that can be at the ottermin antibody also which can give rise to this kind of pattern. But the clue here is that clinical history and lab parameters showing some in some entry markers raising the CSF and symmetrical and diffuse of homogenous operants that is the otterminensia pelletis. Then this Wilson did we all know, we all know Wilson did is that if you see bilateral base anglia thalamine brinsome element and in the brinsome you will see this kind of classical face of giant panda sign in which you will see this kind of high signal intensity in the mid brain segment with the sparing of the red nucleus which gives rise to this face of the giant panda. And there is one more sign which is called as face of the miniature panda which is seen at the content. So when you see this kind of amazing findings with history of geyser flasher wings and history of tremor or behavior changes and is factorial, you can give possibility and you can give appropriate investigations and we can make a diagnosis of Wilson disease. Then moving ahead to there is one more condition which can cause subacute and recurrent encephalopathy or moment disorder and dystonia followed by febrile disease. So this is condition which involves the copper striatum. Here we can see that corded nucleus and putamen. This condition also have this kind of symmetrical or asymmetrical areas of cortical and sub cortical white matter hyper intensities on flare or T2 weighted image as well as cerebral cortex environment. Which can show reduced diffusivity on acute face which can be resolved over time after treatment if we give biotin at appropriate time and you can see that this is the acute phase how the lesions can be angry and swollen and which can have this kind of very well hyper intensity. So there is typical spelling of the gluospalitis as you can notice here and that is the follow-up scan here we can see that there is some residual atrophy and signal changes in the middle of the area are persisting but the cortical gray matter signals have resolved. So that is the common pattern what we see in biotin response in the middle of the disease. So the gene mutation involves SLC19A3 mutation. So this differential we should consider whenever we have imaging appearance of these kind of conditions and we only will be focusing on mitochondrial panel and all. So it's always advisable to also look for biotin time in response to weathering like this. Then moving on to the ADEM. This is the classical examples of ADEM how it can involve. So the usual history will be that the child will have a prior upper respiratory infection one week or two weeks before and if you do CSF the CSF will be undemarcable there won't be any high cells but the child would have operated with encephalopathy which would have been followed by fever or something. Here the lesions will be either deep gray or they can have more of a predominant subcortical. The lesions are poorly defined to fluffy and they are predominant white metal lesions. So when you see this kind of asymmetrical poorly defined white metal lesions which can affect basically also gray matter also then you can raise the possibility of ADEM and it has got good response to zero and the lesions can resolve. The patient those who have ADEM secondary to walk they can have tumor effective or mass forming lesions as we can see here on this second image. Then there are some certain conditions which have which have partial sparing of the regions of the putamen or copper stratum. So it is not necessary that entire putamen or what it should be homogenous to involve. There are certain conditions which can involve a patchy area but that can be symmetric. For example, this is the example of McDonald's syndrome. So when you see this kind of putamenal eye sign so what you are seeing here that there is symmetrical areas of hyper intensity in the bilateral putamen with sparing of the mid part of the putamen. And this patients present with progressive psychobotor regression deafness and dystonia. So when you see in an active case, you will see this kind of mid putamen sparing and that will be a pythagomeric or hallmark for this condition. But when you see this patient later on, later it will then you can see that there is significant atrophy of the brain with also a moment of the mid part of the that putamen which was spared initially. So it is not necessary that when you see this kind of homogenous hyper intensity later, you can exclude Mcville. But if you see in the initial phase, you will see this kind of pattern which is called as putamenal eye sign. Then there are certain micro control or disorders out there. For example, by the way, dehydrogenous complex deficiency, they can involve this kind of posterior putamen at chest and plobus pallidus. Clinically, they have identical neglect syndrome. And here we can see that this is the environment which can so restricted if you're running the acute phase. So when you see this kind of symmetrical lesions, which are restricted in acute phase, you can raise the possibility of this kind of mitochondrial or by the way dehydrogenous complex deficiency. Another example of mitochondrial complex file gene deficiency, which is showing that posterior putamen in a moment, in addition of this kind of brainstorm tracks in moment as you can see surrounding the equiduct of silver, equiduct of silver and surrounding this loss. Then this is one condition that we should not be mistaking as a metabolic disorder, because when we tell that this will be like this, then we are helping the clinician that to avoid unnecessary investigation. As this is static one insult happened happened, whatever damage has was has to be that it has already done. So when you see this kind of classical posterior putamen and metrolateral thalamide in orbit on T2 and flare images. Also, they can involve the posterior aspect of the internal capsule with associated areas of abnormality involving the peri-blonic eye, involving the cortex and subparticle white metal, which in acute case can so restricted different, but on chronic case, they can so volume loss and parent catalytic. So when you see this kind of pattern with classical imaging history or clinical history, if you suggest you have prior insult, perinatal insult or any internal receptor, you can raise possibility of or you can confirm that this is look like more of a perinatal HIE kind of pattern, which is profound. And by that way, we can avoid unnecessary investigation like metabolic or genetic. And that is the one way we can really help to the clinician. So this is also known as chronic type of cerebral palsy. So now moving on to the cluster two of this study. So the cluster two included T2 hyperintensity or increased susceptibility of the globus pallidus. And these are some case examples of the cluster two, which will be going in subsequent slides. So, cluster two had total 85 patients, 85 patients and several conditions and which is listed here, and which consists of so many lysolomal cell disorder to metabolic conditions, as we'll see in a subsequent example. So first we'll start with the globus pallidus T2 hyperintensity without stridal abnormality. So this is a list of conditions that they have provided in the article. So that's a good list of condition when we find this kind of T2 hyperintensity of the globus pallidus, without stridal enrollment, you can refer to these conditions and always look at the entire scan. Is there any other areas in the moment or not. So we'll start with the first of all more common things which can be fine. This is also one condition which is like us, which is, which can have static pose. Because the answer would happen in the unit of time. So that is the current terrace. So the patient will have typically a history of hyper bilimia during the NISO period. And here we can see that the hyperintensity in the globus pallidus is more often diffuse and homogenous T2 hyperintensity. And you should live for other areas of the moment in the case of current terrace. Like for example, subthalamic nucleus in a moment as well as the hippocampi. If these are also in one, then you can raise the possibility of current terrace. So the current terrace in acute changes, they can have even hyperintensity in those areas and they can show a different acute stage, but later state they can have atrophy of those areas and residual globus pallidus hyperintensity. Then another important metabolic condition when you see predominant globus pallidus in the moment only without any other areas of the moment that is the SSADS that is this succinate semi aldehyde dehydrogenase deficiency. And here we can see that initially many of the studies showed that this patient had anterior globus pallidus in the moment. The posterior aspect of the globus pallidus was relatively sped. And there was dented nucleus in the moment also in few of the cases. So when you see this kind of pattern with globus pallidus in dented, you always include SSADS in your differences. And if you timely treat this patient with a VIGA veteran, then you can see that there is also not those hyperintensity which was seen previously. And this condition happens either in late infancy or at least a little bit movement disorders. So this kind of pattern is very important to diagnose this condition. Then moving on to the methyl-melonic aciduria. Methyl-melonic aciduria is also one of the conditions when we see symmetrical areas of globus pallidus hyperintensity. When it is severe it can show cystic changes also and with surrounding this kind of peripheral hyperintensity because of cavitary changes. Methyl-melonic aciduria can be having non-specific finding as volume loss or some very medical hyperintensity. But when we see isolated this kind of GP abnormality in early in life with vomiting, tachypnea, lethargy, seizures, history, we should include methyl-melonic aciduria as a strong possibility. And this patient can have cystic changes or calcification and laterage as we discussed already. The clue we have here is that we can diagnose this condition by doing laboratory tests. So the urinary organic acid or seed profile will show elevated methyl-melonic acid here. So in that way we can come up with the diagnosis. Then another interesting thing is that cerebral creatinine deficiency. Cerebral creatinine deficiency, we all know that many times the MRI findings, conventional imaging will be absolutely normal. But the patient will be having some symptoms and if you do MR spectroscopy that will be the clinching. For example, here we can see that there is absent of the creatinine peak at 3 ppm. So that is almost pathopneumonic for the cerebral creatinine deficiency. Some of this deficiency, they can have globus peridus hyperintensity as shown in this condition, which is more often seen with GAMD deficiency. But the AGAT deficiency with creatinine deficiency, they are having normal scan that we have to see. So the clue here is that we have to do MR spectroscopy also in those kind of disorder to reach up to the diagnosis. Then moving on to the another disorder which can have globus peridus hyperintensity is the cannabinoid disease. So the cannabinoid disease, they can have subquarticle or diffuse white matter enrollment with typical globus peridus thalamus involvement. They can involve brain seven cerebellum also. The disease presents with macrocephaly and hypoteptonia with optic atrophy. And here additionally clue will be that if you do MR spectroscopy, that you will see this kind of mark disproportionate elevation of the anabic. So we have to consider cannabinoid disease whenever we see a macrocephaly child with deep gray involvement, which is sparing the striatum. And if you see some subquarticle white matter enrollment. Another condition which can cause symmetrical GP hyperintensity is current shared disease. This is very important to diagnose. We have to look carefully at the clinical history. When you have cardiac condition defects and patient with having ocular craniosomatic disorder. Like for example, progressive external osteoplasia and having additional retinal pigmentation, then if you see this kind of subquarticle white matter enrollment with symmetrical GP enrollment sometimes this patient can have thalamus and antidepressant enrollment. So when you see this kind of abnormality, you can raise a possibility or add a differential diagnosis in that. So in this study by Dr. Shakip, they have found that kind of sad disease, they can have cystic changes in the tuberous peridus. They found three patients had this kind of abnormality. Then it is not uncommon that we see the hyperintensity involving the pallidum as well as striatum both. So in this kind of both hyperintensity will be having overlapping in cluster one and cluster two. So in that in this study they have found in certain mitochondrial disorders as well as as well as propoenic acidomia and pyruvate dehydrogenous deficiency. However, they went for a literature review to expand this kind of disease abnormality and they found that this many other diseases which can have concomitant pallidol and striatum did to a hyperintensity. Then now we'll move on to the like global pallidus increased susceptibility or hypointensity. So the disorder which includes predominantly are NBIA or NBI mimics. Then certain examples like tube B before or NCL kokens, you know, these disorders have some classical image finding that will be discussed. So starting with the NBIA disorder. So when you see this kind of image with exapiravital symptoms and initially this child can have this kind of symmetrical areas of hyperintensity in the global pallidus. But as the time progresses, you will see the subsequent T2 hypointensity with sparing of the antrometal part of the global pallidus. So that is called as eye of a tiger sign. So when you see this kind of eye of a tiger sign, you will show that this is looking like a peak and that is pentothin. This patient also have this kind of substantia nigra in moment. The susceptibility can be seen at this level also. So the clue is that eye of a tiger, it is a hallmark for this condition. But when you see early, then we can have only this kind of hyperintensity on the middle aspect. And when you see late or late aspect of the same child, you can see that this middle aspect also has been replaced by T2 hypointensity or a supply blooming. So we cannot exclude peak and if we don't see eye of tiger sign, that is the take on point. Then another condition which can have susceptibility is the INED. So this is one of the conditions that we can diagnose on imaging. So when you see on imaging this kind of T2 hypointensity on the global pallidus, which is showing susceptibility on the SWI. And if you see this kind of cerebellar hyperintensity as well as atrophy, we can see that the cranial border diameter of the pharmacy is not reaching up to this OBEX region. So that is definitely atrophy with interpholial space widening. And if you carefully notice that there is relative hyperintensity of the cortex also. So when you see that cerebellar cortex hyperintensity with this kind of finding like global pallidus hypointensity with blooming and drooping of the spring is one of the features in this condition. As well as you can see that the cleaver part will be hypertrophic. So when you see this constellation of finding, you can raise a possibility of INED. Again, in the initial scan, you might not see all the features in this patient as this features you all over time. So like these findings, it is seen that it's petachromonic, but if they are not seen in all consolation, then you cannot exclude the condition. This is the condition which has specific appearance on SWI and T2-metered images. This condition is called as M-PEN. And in M-PEN, you will see that there is a preferential movement of the internal and external part of the global pallidus with sparing of the medial internal medullary lamina, which will be ISO intent or slightly bright. So when you see this kind of ISO intent or slightly bright medial internal medullary lamina separating the internal and external and which are showing susceptibility on SWI. You can raise the possibility of M-PEN in appropriate clinical conditions. And this is the same patient that they have imaged after some time. And we can see that there is more deposition of iron-related T2 high-point density, which can be progressive subsequently. This is another example of NVI that is the B-PEN. So here we can see that in the moment of the substantia nigra is classical, but in the initial scan, they were not showing any susceptibility or any optimal signal intensity. And over the edges, we can see that classical appearance. So this patient have this kind of central hello sign, which is even hyper intense and which will have in this kind of central areas of high-point density. So when you see this kind of imaging appearance, which will have a hello with central band of high-point intensity on X2, D1, M-PEN is in a substantia nigra. That is classical for this condition, which is called as B-PEN. That is the beta-probular assorted neuronal generation, which comes under the spectrum of NVI. Then there are certain disorders, which are NVI mimics. This disorder includes the lysosomal storage disorders, for example, that we'll be seeing in the subsequent slides. So this is the example of fucosidosis, in which when you see the GP high-point intensity as well as thalamic high-point intensity. And high-point intensity can go and involve up to the substantia nigra also. And when you see this patient will have dysphobic feature and on skeletal survey, you will see this kind of skeletal resources in the form of inferior beating of the vertebra and proximal pointing of the metacarpals and so on. So when you see this kind of thing and which shows susceptibility of the globus pallidus on esoblohyuminus, then you can raise this possibility of fucosidosis. So the clue is here that whenever you are seeing lysosomal disorder, there might be underlying T2 high-point intensity. This is another example of lysosomal disorder, which can mimic NVI is the alpha-menocytosis. So this patient, they usually present with prominent forehead, they will have calvaryl thickening and macarocaffelid. They have co-spatial feature as other sorority disorder can have. They present with hearing loss and they will have this globus pallidus and thalamic high-point intensity, which may or may not show the susceptibility on esoblohy. So the idea is that when you see this kind of pattern of high-point intensity and of the thalamic globus pallidus, they can have invariable amount of hypomalination also. And you should always consider lysosomal disorder as a possibility. This is another interesting thing that we can diagnose on the MRI itself. That is the tube before, that is the hypomalination with atrophy of the pituitary gland cerebellum. So what is happening in this patient that there is relative hypereintensity, subtle, there is mild relative hypereintensity of the entire white matter of the cerebral hemisphere. It's not marked as we have seen in other dysmyelinating lipo dystrophies like L2-hydroxyglutaric acid today, our cannibal. It's just a mild relative hypereintensity. And in this disorder, what happens that the caudate and butamen, they will progressively atrophy. So the bitter English or progressive atrophy, but the initials can have this kind of T2-hypointensity of the globus pallidus and thalamic. This is relative hypereintensity because there is no white matter malination, so they stand out. So that's the reason why we see this kind of apparent hypereintensity of the globus pallidus and thalamic. This patient also have this kind of cerebral atrophy as we can see here. So when you see this kind of constellation, then it is diagnostic of tube BV4 hypereintensity with basal gland cycle. So that leads to a few conditions that they have provided in the article on chart, that which are the conditions which can have T2-hypointensity in the thalamus. So these are the some conditions which may not be completely because every year we come across even pathology which can have same kind of spectrum. And these are the disorders which can have hypereintensity with basal gland cycle. So these conditions you can go through this article. It is available online. Then there is one characteristic finding called wishbone kind of appearance on SWI signal intensity in late onset or type 3GM1 gangiosatose. So when you see a patient with this kind of skeletal resources with posterior putamen and susceptibility of globus pallidus which is having this kind of wishbone kind of appearance, then it can be late onset or type 3GM1 gangiosatose which is almost pathognomonic for these conditions. There are certain disorders which you will have marked cerebral as well as cerebral atrophy. And because of this atrophy and neurodegeneration they can have this kind of hypereintensity of the globus pallidus and thalamic as you can see here. This patient also have this kind of periwet riddle of limb of hypereintensity and thinning of the corpus callus and this cerebral atrophy. And on MRS we can see that there is induction in DNA. So when you see this kind of group of condition or group of findings, this is seen in the NCL. So clinically this patient have heterogeneous clinical recognition. So this kind of imaging finding can aid value in diagnosing the condition. So this patient other hallmarks clinical findings are visual impairment and cognitive impairment. And when you see this kind of diffuse marbed gray and white matter atrophy in cerebral hemisphere with cerebral atrophy with this kind of T2 hypotense GP and thalamic always think as a NCL as one of the possibility. Then this is another patient who can have a variable degree of hypomalination or white matter abnormality. But the patient, if gives, there is history of cuteness, photosensitivity, dwarfism and approach it all like faces. When you see this kind of imaging appearance of variable hypomalination or white matter signal intensity abnormality with susceptibility on SWI, which is calcification in the middle of Anglia with cerebral atrophy. Then this condition is called as cocaine syndrome. So when there is a classical clinical abnormality with this imaging manifestation, we can raise this possibility. So there are certain conditions which can have a cerebral atrophy with vision and glasses ability. And these are the examples of those conditions that you can see. And we want to the our cluster three, that is the T2 hyper intensity in the global spell it is brainstem cerebellum with restricted division. So here they found this disorders and the examples predominately were the white matter in toxicity and crevices and so on. So this is the example of why I've written toxicity, which is involving and showing restricted different in the global spell it is telling us symmetrically, and also involving the brainstem tracks and the internet nucleus. Another additional finding in viability toxicity is that they can all the hypothalamus in all the case. So when you see hypothalamus in moment with this kind of a symmetrical finding, and you have to take care that is there any free of my government in tech. And the drug is useful mainly for the infantile spasm. And these are the classical features that we can see under viability toxicity. So that leads to, there are certain conditions which can involve hypothalamus with 32 hyper intensity and these are the certain conditions out of which viability is one of them. Moving on to the another case is the crevice disease, which can have global spell it is a brainstem track in orbit, which can show restricted different in the acute event. And the hallmark feature would be that there will be disproportionate atrophy of the brain parent camera for the age, and you will see this kind of white matter hyper intensity in the parietal occipital or frontal parietal regions. They will have abnormality in the bleak as well as corticospinal tracks in the brainstem, as well as cerebellar in the homing. This patient also can have the two hyper intensity of this LMI. And if you do CT you will see some sort of hyper density in the LMI in these patients. So the presentation of this condition in the child would be this patient will have a hyper irritability and aggression in an early infantile phase. And that is the, these are the hallmark features of the infantile variety of crevice disease. And there are many other varieties which which can be juvenile or adult which I am not taking, but the infantile variety will have this kind of imaging finding. And this is the findings which can have optic track technique. I forgot to mention that crevice is one of the disease which can have this kind of optic asthma technique which we have seen in a disorder like Alexander can have. Even now MLE and some other conditions like ADM in acute phase can have optic track technique. These are some other ophthalmic abnormality which can have some other several conditions that we can call it at your ease. And then moving on to the last cluster that is the prominent even hyper intensity without accompanying T2 weighted abnormality or DWI. So in this age group, they observed the T1 hyper intensity which was predominantly seen in hyper magnesium group in those and they had found this kind of gene abnormality SLC30A10 and SLC39A11 gene abnormality in those conditions. So one of the example is this manganese transport defect that is SLC30A10. So what we are seeing here that there is diffuse hyper intensity of the entire viscera ganglia involving the corret, putamen and globus pallidus that we are not able to distinctly see the boundaries between them. And this patient also have this excessive hyper intensity in the corpus callus. They can also have hyper intensity in the buttery gland itself. If you see the brain stem there is a characteristic ventral sparing and also hyper intensity in the brain stem. So as the cerebellar white metal, you know, so when you see this kind of involvement, you should always look for manganese transport defect. This kind of changes they may not have susceptibility or T2 hyper intensity. So that is one way to differentiate from other disorder like India and other conditions like recent disease. This is an example of SLC39A14 that is also a manganese transport defect. So the findings are limited only to the globus pallidus, but in severe cases it can go and involve to the other part of the brain as well. So even hyper intensity that can be diffused, which is labeled as S category and this are the reasons for the diffuse hyper intensity, which includes hyper magnesiumia. Sometimes it can occur in Wilson disease or toxicity due to aphid drying. And sometimes the hyper intensity can be big patchy and the patchy hyper intensity can be due to this angle of calcification or a sick will or some prior inflammatory disorders and certain poisoning. Then winding up last category that is the disorder with this angle of calcification. So this angle of calcification can be seen in primary disorder or that can be secondary to some systemic disease or metabolic disorders as mentioned in this table. Or sometimes they can be associated with the monosinic disorders like ADAR, certain metabolic disorders like falling deficiency and so on. Here is the example of calcification. Unfortunately, we don't have CT to show, but here we can see that there are alter signal intensity in bilateral visor anglia and susceptibility in the globus pallidus. But here we can see that it's kind of patchy areas of SNF like looming and gory nucleus and glutamine as well, plus dented nucleic acid element. This patient had low calcium and metabolic arrangement was there and that was history of titanium painful muscle spasm. So on further workup it came out to be hypoperatism. So the clue is there that when you see this kind of stridal and globus pallidus patchy patchy areas of involvement which shows susceptibility. So keep consideration of metabolic disorders like involving the calcium disturbance in your mind. So this was the discussion about the different clusters and their disease conditions. So they had this kind of condition but with further review of literature they also added few more 59 disease category based on again the signal changes and differences. So they also had included certain adult categories because they can predominantly involve the visor anglia and they can show susceptibility on SWI like as I don't know. And the mitochondrial disease they have grouped as a distinct syndrome that we saw as a consign syndrome or medial or they have separated amongst the complex effinency in this article. Finally they came up with an algorithmic approach how to handle bilateral visor anglia abnormality in which we have to start first with whether the abnormality is seen on T2 weighted and it is showing hyper intensity of the visor anglia or restricted effinity on the visor anglia. So when it shows the hyper intensity or the effinity section then we have to carefully see whether it's involving the striatum part that is caudate of butamine or it is involving the globus pallidus part. So when it is involving the striatum part only and if that is yes, then you can see the cluster one and those kind of conditions and associated patterns that we have already seen. And if it comes to know that it may not be knowing only the striatum, then you have to go to the overlapping patterns that we already discussed that certain condition can have pallidum as well as striatum. And you can go into that those kind of differentials. Same when you see T2 hyper intensity only in globus pallidus and then you have to see that category I in that table to that I already shown you that certain conditions which is only affecting the globus pallidus and which is having bright signal intensity on T2 weighted in this. And you can differentiate based on other features and clinical information and further genetic testing. So that was about the T2 hyper intensity. When you find T1 hyper intensity in business then you have to see that whether the abnormalities are patchy or diffused. If it is patchy then you have to go to differentials of the patchy T1 hyper intensity which has been which I have shown earlier in the previous slides. And when the hyper intensity is diffused and but there is no susceptibility then probably you are dealing with that manganese disorders and you can go with that pattern. But if you see that T1 hyper intensity with SWY susceptibility, then you have to see that which are the areas which are involved. If globus pallidus, substantia nigra and subthalamic nucleus is involved, then you have to see that what is the additional neuroimaging features. For example, is there any hypomalination that we have seen few examples of hypomalination with globus pallidus. Is there any optic atrophy or is there any salivarytrophy? And you can go and look out the causes which can affect those conditions. And you can also say there are certain conditions which can have T2 hyper intensity of thalamus. You can go according to that chart also. And if the viscigal is showing susceptibility which is predominately in striatum that is considered as category R that we will be seeing in the next slide. So here is the example of viscigal hyper intensity which can affect predominately the striatum which is seen in more of an adult age group that is the A cerebral plasmid mermia. And here you will see extremely low or undetectable level of cerebral plasmid. And you will see elevated ferritin and this iron is activated in this kind of specific structures in the corpus striatum and thalamine. They can affect the cerebellar cortex and grimator also. So when you see this kind of condition you can raise possibility of A cerebral plasmid mermia which is seen usually in the adult age group. And there are some other disorders which can have susceptibility of striatum and this is the list of that thing which is also available online and you can go through that literature. So they have also done this kind of same data representation online and you can go on this website called Gates Neuroscience in which they have tried to make an electric tool to examine differential diagnosis. By little bit like a software and when you click on this you will be given option of pressing on this button that is called MRI diagnostic tool. When you press on that you will be seeing this kind of window in which instruction will be provided and you can go into that MRI findings column and in MRI findings you can and roll your data for case data data that which are the structures which are involved and whether they are hyper intense or hyper intense. Is there any other areas of involvement that we have subsequently seen in previously and so on. If you mark this areas the software automatically will give you that this highly probable differential diagnosis or like which condition can have this kind of abnormalities. So if you go on to particular slide they have also provided some a few particular features about those conditions and and many of the disease has got this kind of imaging appearance also so that's a very useful software which is freely available online on that on that article link only. Before we go to summarize clustering of the neuroimaging patterns will help in complimenting the clinical information and that will aid in differential diagnosis and guiding the diagnostic testing, and it's a useful approach, useful approach to see the pattern recognizing, and once to you recognize the main pattern like for example, whether it is predominant globus pelatus or predominant stridal nomen, whether it is showing increased susceptibility or not, or it is showing even if it's hyper intensity, then you have to look for other clues on MRI. Whether it is isolated finding or it is combined with some other structures in the moment, which that will tell you to further narrowing out the differences, and there are certain disorders like MSUD, KNMN, type of metharic aciduria, anac, L2 hydroxy, letharic aciduria. These are the disorders they have typical imaging findings so that we can diagnose on imaging and we can be very confident. But in certain conditions like conic terrace and monoxide toxicity, the findings may not be specific, but here you have to take into consideration of clinical history and that will help you out. So first and most thing is that you have to thorough examine the child and have proper clinical information. And by this way, pattern recognition, we can be useful in evaluating some unrecognized in order and we can use full opinion and proper agnostic testing. So by that, I would like to conclude today's article and thank you for listening to this article. I would like to thank the Department of Radology, CMC Vellore, in which few of the cases I had shown here when I was doing my periodic redolyphalogy. I would like to thank the Department of Radology and Ecstasy and Dr. Asik Biswas who had made a wonderful pattern based approach on based on a disorder during his CMC tenure. Thank you. And I would be happy to take any questions. Thank you, Dr. Hireen. That was an excellent article and it took us to us really beautifully. Basically, Anglia disorders are very commonly seen in pediatric neuroimaging and I'm sure the way the approach that you've shown us will definitely help us guide the further course of management also as to what investigations also genetic testing and the algorithmic approach that you showed I'm sure will definitely help us. I hope we take the questions. I would like to invite Dr. Deepak Patkar sir to kindly address the delegates. Thank you, Hireen, for fantastic presentation. It was really, really good. Especially the approach and the pattern. That's something that people should remember and software, the artificial intelligence would reduce their intelligence. We should reach there first. Sir, you're not audible. I think he got disconnected. He's just reconnecting. Yeah, okay. Dr. Hireen, there are a couple of questions. So let's take those questions after sir's address is done. Okay. And we've shared the link for the article in the chat box for those who want to go and view the article. And if you have any questions, I'm sure. Sorry, sorry, sorry. Yes, yes. The Wi-Fi went out. So thank you. Thank you, Hireen, for a fantastic presentation. They are friends and colleagues. It gives me immense pleasure to be addressing you on this platform of Indian Radiologist, the Radiology Journal Club. It's a novel initiative by Indian Radiologist. This is an endeavor to keep young radiologists updated. This is our fifth Radiology Journal Club. In this monthly event, we discuss a recent relevant radiology article, followed by case discussion. That's what you read today. I would especially thank his valuable time and contribution to this extremely difficult talk and approach. He has systematically taken all the delegates through a very important topic in a very, very abusive manner. To the people present in the webinar, thank you all for keeping up the enthusiasm to understand new things, learn and improve your knowledge. Learning is never complete and you'll always find something new to learn every day. That's what I feel and that's what I practice. I would like to acknowledge the efforts of everyone from Indian Radiology, especially Dr. Gowri, Dr. Mitusha and Dr. Mitputkar, for keeping this alive and cooking. Do join us for our several upcoming dedicated telemedicine sets of masterclass studies focused on Brest, Onco, MSK and community radiology. We are also trying to do something on fatal imaging. So, especially all of us know is the way forward and we at Indian Radiology are trying to do that in a very systematic manner. Links will be shared on Indian Radiology's webpage and of course on social media platforms. Thanks once again, all of you, for being part of today's endeavor. Stay safe, stay connected. Thank you, Gowri and Mitusha. Thank you, sir. I would just like to say thank you, Pat Kursar and the entire team at Indian Radiology for providing us this platform and coming up with such innovative ideas like the Journal Club. And I hope this goes on forever. So, thank you so much. Dr. Giren, I think we can take the questions. There are a few. There's one which says when, when will we say GP Global Global Spellidus Substantia Nigra is hypo on SWI. Any reference? Yeah, yeah. Yeah. So, there is one article on Agent R they have said about this susceptibility weighted imaging on Global Spellidus specifically. Your question is very valid and that is very difficult because even when the child in different age group, they will have some sort of, if you see on SWI sequence, you will see some low-signal intensity in those areas. It will not be apparent in the children less than five years, but as the children goes more than 10 years, you will see some sort of more like SWI, high-point intensity kind of area. So, the thing is that you want to ask the men to tell pathology and men to not. So, that's a difficult, that's more of a eyeballing and that will leave your machine specific thing. And but there are certain clues that will help you. The thing is that if you see only some peripheral high-point intensity, which is symmetrical and well-defined and which is progressing gradually centrally, that is called as normal SWI high-point intensity on the Global Spellidus. So, that should not be labelled as pathological, but if you see some sort of spotted abnormality or speckled or inhomogeneous appearance on Global Spellidus, which is many marked, then you can say that this is looking abnormal or pathology. Otherwise, if it is symmetrical and like some sort of linear, which is centripetal, like from periphery to central gradient kind of thing, then it is more likely to be artifact or it is like three tesla related changes in which can be seen on SWI sequences. I hope that answers your question. There's one more question, which says, is there any criteria to say Wormian etrophy? Yeah, that we can definitely say. So, basically, I would like to show you that Wormian etrophy, any case. So, if you see this particular image, NCL, so ideally the superior Wormy starts from this colloquial level and it should end till the level of optics in a normal population. So, when, if you draw a line from the optics and if it is not reaching, the Wormy is not reaching up to that level, and if you see some interpholial space widening that is seen here, then you can tell it as a Wormian etrophy. And if you don't see interpholial space widening, but if you see that volume, Wormy is small in size, it is not reaching up to this optics area, then you can, that could be Wormian hypoplasia. So, that's the difference between Wormian etrophy, Wormian hypoplasia and normal finding. One more question, the ideal TE value for MRS in units in metabolic mitochondrial conditions. Ideally speaking, units can have those kind of amino acidopathies and organic acidurias. So, ideally it should be done in both 35 as well as 144 TE. That is the low and intermediate TE, because the low TE will become the smaller amino acid, which can be seen only at 35 TE, which will be obscured at intermediate TE. But if you're looking for mitochondrial and those kind of disorder, it is preferably or it is ideally recommended that we should do 144 TE also just to look at that inverted electric peak to be more confident about that. And in older children, what I have seen that MR spectroscopy at 140 40 will would suffice in most of the cases. If we are lack of time. Yeah. Yeah, I think someone's asked for the websites slide again. Can you share the websites slide again. Okay, I'll slide. So, when you type on Google, this MRI patent based approach, you will see this article, this by Dr. Shakib and and if you open, they will be showing that the data availability and they would have given this link kidsneuroscience.org when you click on this link. If you open a new window that is the kidsneuroscience center in which they have given this electronic tool to examine differential diagnosis. And there is a one link for that tool. So you have to press this diagnostic tool that will download in your system. And then you will be opening a new, a new window will open. This is the that software or artificial intelligence tool in which you just have to go to the MRI findings. You have to mention that what are the structures which are involved. And you will see that any other areas of enrollment, even hyper intensity, hyper intensity, susceptibility, all kind of information they have put here. You have to click just that thing and based on your clicking, the computer will give you a certain disorder that can have similar structures of enrollment. And then you clinically correlate that which are the things which are best fitting with those kind of just to tell you that this study also had limitation because the study population was only from the distinct Sydney UK mainly and those kind of population and it has done only the MRI available to them during those time. The thing is that this metabolic disorders and certain conditions they evolve over time and the classical imaging features they can evident later in the same patient. So you might not see the same finding if you scan and patient early. So this may not be absolute software, but it's a good try to see some differentials. For example, they had very few cases of infective encephalitis involving the poison and all, but I would expect that if it was India, we would have expected more of an infective encephalitis involving the poison India. So that kind of changes will be there, because we have different cohort of patient in our population. Yeah. There's one more question. How to differentiate leaves from pandas imaging wise. Imaging wise, it's difficult. It's difficult because some if it is symmetrical. And if it's showing this kind of subtle necrosis which can happen in both of the conditions. It is difficult, but if the lakes is having some other findings like involvement of the subthalamic nucleus involvement of the brainstem tracks, which are which are very equitable or involving the substantia nigra, then you can confidently say that it's like more of a leak. This is secondary to micro control. In that also the subthalamic nucleus is more commonly involved in in cox deficiency or self mutation. But if in unknown case with only that basically abnormality which is symmetrical, you have to more reliant clinical finding rather than imaging. Other thing you can try out the MR spectroscopy and in different era, which are not swinging. If you are seeing some sort of like that big in normal living areas, then you can say that might be leaks. This is secondary to micro controls. And I think that covers all the questions. Thank you once again for really taking that and for your time on a Sunday morning. Thank you so much. We will share. I'll try to share the link once again in the chat box. I think a few people are not able to open the link. And I'm sure if anybody has any questions, they can always reach out to you, Dr. Hiren. Yeah, they can always reach out. I'm sorry, I have not put my email ID, but it is in the chat box. That's also fine. Yeah, I'll just share my email ID. All these videos will be available on the Indian radiologist YouTube channel as well. So please do visit the website and also check out the channel. Also for more academic videos, similar videos and all the radiology journal club videos are also available so you can go and check them out later. And if you have any queries, any doubts, you can always reach out to any of us, me, Dr. Mitusha and the other speakers who have been with us so far. Thank you everyone once again. Thank you, Dr. Hiren. Thank you so much. Thank you once again for inviting me. I hope they could have learned something from this lecture. I'm sure they must have. There will be a lot of positive comments also coming up. So thank you. Thank you. Dr. Amit, we can have the sponsor videos once more please. We'll see you all next month with another journal club. We have taken the highest customer satisfaction rate over the years with our highly experienced and exceptionally qualified leadership. We have become a trustworthy organization in the industry. 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