Good evening everyone. Thank you for joining us. I know the program is announced in very short notice. But thank you for taking the time from your busy schedules and joining us for this pollute. So in case any of you don't already know, this is a pollute for the International Edition of the MRI teaching course which will be happening on the last weekend of October and the first weekend of November. So for those of you who haven't already registered, please register. It is a five-day program. We have speakers from across the world including the Mayo Clinic. We have speakers from Canada, England, all across the US, Australia, Singapore. And we also have an entire day organized by Dr. Dushan Sahani who was the chief of radiology at the University of Washington. And his entire department will be taking us through how they run their MRI practices. So starting off today's pollute session we have Dr. Alok Jhaju. His topic for today is congenital CNS anomalies. He's a pediatric neuro-radiologist at the Loody Children's Hospital of Chicago.  Hello everybody. It's a pleasure to be speaking at this MRI conference today. My topic here is congenital CNS anomalies. As you know it's a very broad topic and in the next 30 to 35 minutes I'll probably barely scratch the surface. So for this case-based review what I have done is I have focused on a few selected entities and I will start with showing an uncommon presentation of that entity and use that as a launchpad for a general discussion on that particular condition. So let's get started. So the first case is a 15-month-old who presented with seizures. On these sagittal D1-weighted images we can right away see absence of the corpus callosum and then there are these multiple salsae which radiate all the way up to the ventricular margins. On the coronal images there is absence of crossing fibers, abnormal ramson orientation of the frontal haunts, a high-riding and dilated third ventricle. Similarly on the axial D2-weighted images there is absence of crossing fibers in the midline with a prominent intahemispheric fissure. But the patient also has many other abnormalities including these multiple cysts in the lateral ventricles and possibly in the intahemispheric fissure. Now you can also see those cystic structures on this sagittal D1-weighted image. Also the cortex and the gyral contours are very abnormal with broad gyri and shallow salsae in the right frontal region associated with this large mass-like area of grey matter heterotopia. So what is this constellation of findings called? Is it a Cardi syndrome? Is it a Cardi Gutierrez syndrome? Is it Cleoneuronal tumor based on the cystic changes? Or is it Miller-Dyker syndrome? So this appearance is diagnostic of a Cardi syndrome. So a Cardi syndrome is one of the syndromes associated with corpus callosulitis genesis and it has the associated findings as we saw including grey matter heterotopia, polymicrogyria cysts and sometimes posterior fossa anomalies as well. It is a real developmental disorder which is caused by an excellent defect. So it is fatal in males and only manifests in females. Clinically it is characterized by infantile spasms and on a fundoscopic exam you may see coriorentinal lacunae. A few words about corpus callosulitis genesis. So corpus callosulitis genesis is one of the most frequent plane malformation. It can be complete absence of corpus callosum which is called a genesis or partial absence or disgenesis. It is often associated with genetic abnormalities either trisomies or some single gene mutations or can be associated with extrinsic factors like maternal alcohol syndrome. And as you know corpus callosulitis genesis is often associated with other intracranial and spinal anomalies or craniofacial anomalies and a lot of them have syndromic associations. This is a companion case. This is a 17 year old male with developmental delay and seizures. On the axial T2 and T1 weighted images we see this lobular hyper intense mass in the midline in the expected location of the corpus callosum. Also there is parallel orientation of the lateral ventricles. On the sagittal T1 weighted images we see this lobular T1 hyper intense mass in the region of corpus callosum which completely suppresses on fat saturated sequence. This is an enhancing vessel through that region. So the findings are suggestive of a peric callosulipoma with disgenesis or absence of corpus callosum. So peric callosulipoma it's the most common location for an intracranial lipoma. It occurs in the inter hemispheric fissure and it is closely related to the corpus callosum which is often malformed. There are two morphological subtypes of peric callosulipoma which include tubular nodular which is the more common like in our case and it's often associated with severe corpus callosulitis genesis. The other subtypes is curvilinear where you have a thin band of fat along the corpus callosum and the corpus callosum may be either normal or only milder genetic. There can be other associations with this including absence of tympilocidum, azagus, ACI, polymicrogyria, heterotopias or sometimes dorsal cysts. Moving on to case number two. This is a one month old child with dysmorphic features. So on the axial T1 weighted images we see this abnormal fusion of the cerebral hemispheres across the midline. The inter hemispheric fissure is partly present, it's present anteriorly and a small portion is present posteriorly but it's obliterated in the midline. And you can see the continuation of gray matter and white matter across the midline as well as this abnormally long sylvian fissure which continues across the midline over the vertex to extend on to the contralateral side. Same findings on the coronal images, there is fusion of the cerebral hemispheres in the midline, there is fusion of the ventricles with absent interventricular septum and on the sagittal T1 weighted images we see absence of corpus callosum for the most part. So what's the diagnosis here? Is it schisencephaly, is it scintillencephaly, is it semilobar holoprosencephaly or is it arinencephaly? So this is an example of scintillencephaly which also goes by the name of middle inter hemispheric variant of holoprosencephaly. So what is holoprosencephaly? So holoprosencephaly are characterized by incomplete separation of hemispheres due to abnormal cleavage of the prosencephalon. It's often associated with other midline anomalies including anomalies involving corpus callosum and the hypothalamic pituitary axis and also associated with grinofacial malformations. Holoprosencephaly is a spectrum with the least severe form being alobar and the most severe form being alobar and the least severe being lobar. Middle inter hemispheric variant is somewhere probably between semilobar and lobar. So in alobar holoprosencephaly there is a single midline forebrain with a horseshoe shape monoventric and a dorsal cyst. In semilobar holoprosencephaly there is some separation of the hemisphere. The inter hemispheric fissure is partly present posteriorly and there is fusion anteriorly. There is variable degree of deep nuclei and thalamic fusion in semilobar. And lobar holoprosencephaly is the least severe form where there is only fusion of the most inferior portion of the frontal lobes otherwise the hemispheres are separated. So this particular case is the middle inter hemispheric variant of holoprosencephaly which is a relatively milder form. And there is cerebral fusion in the posterior frontal or the parietal region with partial presence of inter hemispheric fissure anteriorly and posteriorly. There is a horizontally oriented silver fissure that extends across the midline over the vertex. The corpus callosum is usually abnormal with the body being absent and the genus and spleenium are present. So holoprosencephaly are kind of the exception to the rule of colosal disgenesis in terms of its embryological development. This is an example of semilobar holoprosencephaly where you see fusion of the frontal lobes across the midline. There is absence of interventricular septum but the inter hemispheric fissure is partly present posteriorly. Again you can see the same findings on T1 weighted images. There is this band of gray matter along the anterior aspect of the ventricles. There is absence of the interventricular septum and fusion of the frontal lobes across the midline. On the sagittal images we can see absence of the corpus callosum in the mid portion or the portion of the spleenium and probably the genus are present. This is an example of alobar holoprosencephaly where there is lack of separation of the cerebral hemispheres. There is a single forebrain with a horseshoe shape monoventricle which widely communicates with this large dorsal inter hemispheric zest. Moving on to case number three. This is a child who presented with seizures. So on MR evaluation we have coronal and sagittal T1 amperage sequence. On the T1 weighted images we see this abnormally thickened and lobular appearing cortex in the right perisilvian region as well as in the left perisilvian region. Also on the sagittal images we see this abnormally deep sylvian fissure which extends all the way up to the vertex and is lined by these thickened and lobular appearing cortex. Same findings on T2 weighted images you see abnormally thickened and lobular cortex in bilateral perisilvian region. Also there is absence of septum pellicidum. So what's the diagnosis? Is it schizencephaly, polymicrogyria? Is it focal cortical dysplasia type 2 or is it gray matter heterotopia? So this is an example of bilateral perisilvian polymicrogyria. So polymicrogyria is characterized by numerous small gyri with bumpy appearance of the gray white contour. It is caused by the arrangement of neuronal organization and abnormal cortical lamination. It can be sporadic or can be genetic or sometimes may be associated with inutrient infection or vascular insults. There are multiple syndromic associations with polymicrogyria and on imaging it can be focal, multifocal or diffuse. So bilateral perisilvian polymicrogyria is one of the common presentations. It can be sporadic or familial. It presents with developmental delay, motor deficits and sometimes seizures. There is a MR grading system for perisilvian polymicrogyria. So grade 1 is the most severe where you have involvement of perisilvian region as well as frontal or occipital lobes and abnormality reaches all the way up to the frontal or occipital poles. Grade 2 is where the polymicrogyria extends into the frontal or occipital lobe but does not reach the poles. Grade 3 is purely insular and ocular in region involvement like we saw in our case. And grade 4 is the least severe form where you have involvement only of the posterior insular bilaterally. So these are two cases showing focal polymicrogyria. So the patient on the left side has this almost mass like lesion in the left frontal lobe with multiple lobular areas of gray and white matter. So this is an example of a complex nodular polymicrogyria which can mimic a mass but it does follow gray matter signal on all the sequences. This is another example of focal polymicrogyria where in the left parietal lobe we see an abnormally deep sulcus and a thickened lobular cortex lining the sulcus. So that can, again, this is something that can cause seizures and needs a careful evaluation of MRI for diagnosis. This is an example of diffused polymicrogyria, a young child, a few months old, presented with infantile spasms. So on the T1 and T2 weighted MRI we see this abnormal gyral and sulcal pattern bilaterally. The gyri are abnormally white, the sulci are shallow and there is this nodular lumpy-bumpy appearance of the gray-white junction throughout. So this is an example of bilateral diffused polymicrogyria. Moving on to case number four, a three-year-old female presenting with seizures. So on the axial T2 and T1 weighted images, again, we see this abnormal gyral and sulcal pattern that is broadening of the gyri and very shallow sulci. And there is associated thickening of the cortex. If you look more carefully in the posterior region, there is this band of white matter which separates somewhat normal appearing cortex with this additional band of gray matter looking tissue. So defining is probably seen a little better on T1 weighted images where we see posteriorly a relatively normal thickness of the cortex, a band of white matter and then another band of gray matter. And anteriorly it looks more like diffuse cortical technique. So what's the diagnosis? Is it polymicrogyria? Is it gray matter heterotopia? Is it focal cortical dysplasia type 2 or is it age area? So this is an example of subcortical band heterotopia. So subcortical band heterotopia belongs to the lesioncephaly spectrum of disorders. So lesioncephaly are characterized by smooth brain. There is paucity of gyri and sulci and associated thick cortex. It's on a spectrum. So age area is the most severe form of lesioncephaly where there is absence of a sulcation and the brain has a very smooth appearance with shallow silver and fishes giving it an hourglass appearance. Or the milder forms is called the package area where there is decreased number of gyri which are abnormally broad and shallow sulci. And package area can be associated with subcortical band heterotopia. So lesioncephaly is caused by arrested neuronal migration and the cortical lamination is abnormal with four layered cortex instead of five. There are two important genes which are involved in lesioncephaly spectrum. The first one is the LIS-1 gene. It's the most common either deletion or mutation of this gene can result in lesioncephaly. The other is XLIS or the DCX gene. It is an X-link disorder which causes lesioncephaly in homozygous males, but it causes subcortical band heterotopia in carrier females. So our case was a three-year-old female who had a package area with subcortical band heterotopia. This is an example of what's called the classic lesioncephaly where you have a smooth brain with diffuse lithic cortex and very shallow silver and fish are giving it a figure of eight appearance. This is another example of lesioncephaly, but in this case there is associated mycroftalmia and retinal detachment. So this constellation of finding is called the Miller-Dyker syndrome and this is associated with LIS-1 mutation. Another variant of lesioncephaly which is sometimes called lesioncephaly type 2 is the cobblestone lesioncephaly. Again just like any other lesioncephaly there is reduction in normal salcation, but in addition there is a bumpy appearing cortical surface which gives the name cobblestone lesioncephaly. This is commonly associated with the muscular dystrophy syndrome which also go by the name of alpha-dystrocliconopathies and these include conditions like Walker-Wartburg, Foucaillam, and muscle-eye brain disease. So on imaging we may not be able to distinguish between these individual subtypes so what we can call on imaging is a Walker-Wartburg imaging phenotype when we have all of these findings present. So let's look at an example. So in this patient we have this diffuse paucity of cells in both cerebral hemispheres with a smooth appearing cortex with a smooth appearing gyri, but there is this lobular morphology to the cortex. So that's the characteristic of cobblestone lesioncephaly. You can see it a little better in the paritoxibital regions. There is associated marked ventricular megaly and this characteristic kink appearance of the brainstem with associated cerebellar hyperplasia. There may be some mild cystic changes in the cerebellum as well. This patient also has abnormalities of the eye in the form of persistent hyperplastic primary vitria. So this constellation of findings of cobblestone lesioncephaly, colosal dysgenesis, ventricular megaly, abnormally kink brainstem, hyperplastic cerebellum, and ocular anomalies is associated with the Walker-Wartburg phenotype. Next case is a five-month old who presented with nasal obstruction. So we have a sagittal D2 and D1 weighted image, which shows a bilobed mass extending into the nasal cavity. Superially, the mass appears to communicate with the subarachnoid space via defect in the cryptiform plate. Same findings on the axial and coronal images and on the post-contrast images there is enhancement of mucosa surrounding this cystic mass, but there is no enhancement within the mass itself. So pretty straightforward diagnosis. Is it a cephalosil, a nasal dermoid, nasal glioma, or an inverted papilloma? So the diagnosis in this case is a cephalosil. So cephalosil is congenital herniation of one or more intracranial structures through a defect in the skull. And depending on the contents, it could be a meningocil, which contains meninges and CSF, meningoencephalosil, or simply encephalosil, which contains meninges, CSF, and brain parenchyma. Cephalosil is a more general term which includes both meningocils and meningoencephalosil. And then there is a variation of cephalosil, which is called as atretic parietal cephalosil, which is typically seen in the midline hyperietal region, and is characterized by herniation of meninges and some fibrosis or dysplastic tissue. Location, it can occur in the posterior location, either in the occipital or occipital cervical region, and this form of occipital cephalosil is more common in the western countries. Or it could be frontoethmoidal, which is called the sensipital cephalosil, which is more common in Southeast Asia. So frontoethmoid cephalosil can also be classified into two types based on the bony defect. It could be nasofrontal, as in this case where you have herniation between the frontal bone and the nasal bone, or it could be nasoethmoidal, where you have herniation between nasal bone and the nasal cartilage, like in our case. This is an example of occipital cephalosil. So we have a large bilobacillic mass arising from this defect in the occipital bone. There may be some herniation of brain parenchyma through the defect. Intracranially, we see a basement of the extra axial spaces, mild dilatation of the ventricles, and abnormal morphology of the posterior fossa structures, including a small posterior fossa effacement of the cisterna magna, inferior herniation of the cerebellum and crowding at the furum and magnum. So these findings are reminiscent of a Kiari II malformation, but when you have a cephalosil with findings similar to Kiari II, it's called Kiari III malformation.  They are in the inferior occipital or the occipital cervical region, but in our case it was more in the superior occipital region. This is an example of a broad-based parietal cephalosil, where there is a large bone ed effect in the parietal bone and herniation of both the cerebral hemispheres through the defect. There is also some cleosis in the herniated brain parenchyma. And this is an example of a tritic parietal cephalosil. Like we previously said, it's most commonly seen in the midline parietal bone and it's characterized by a herniation of meninges and some dysplastic tissue, but there is no herniation of brain parenchyma or dural sinuses. There is typically abnormal orientation of the straight sinus, which is more vertical. There is a persistent falcine sinus. And then there is this cigarship CSF cleft, which extends from the supracerebellar system all the way up to the defect in the calvarium. And also in this case, on the hemorrhvenogram images, we see this focal splitting of the superior sagittal sinus, which is related to where the tract bisects it to reach the defect in the calvarium. The next case is a spine case. This is a one month old child who presented with the sacral subcutaneous mass on the sagittal and axial T2 weighted images. We see this, we see this racism of the sacral region and we see the cystic mass, which appears to be contiguous with the distal spinal cord. Here again, you can see the distal spinal cord with the cystic mass contiguous with it. There is no associated lipoma, although there is some continuity of the epidural fat with the, with the subcutaneous fat. The important thing to note here is this is a close defect that the cystic structures is completely covered by skin and the subcutaneous tissues. So what's the diagnosis here? Is it a myelomaningocele? Is it a myeloskesis? Is it a myelocystocele or is it a dermoid cyst? So the correct answer here is myelocystocele. So myelocystocele is a closed neural tube defect where you have herniation of the dilated central canal or the syringocele through a defect in the posterior elements. Here is a diagram illustrating the myelocystocele. So you have dilatation of the distal, dilatation of the spinal canal, which is called a syringocele and the syringocele extends through a dysraphic defect in the posterior elements. And since it's a closed neural tube defect, the cyst is covered by skin and subcutaneous fat. So it's a rare form of closed or occult spinal dysraphism present with skin covered subcutaneous mass, as in our case. It's most commonly seen in the sacral region where it's called the terminal myelocystocele, although it can be seen in the cervical thoracic region where it's called the non-terminal myelocystocele. This is an example of non-terminal myelocystocele where we have this dilated central canal extending into this fluid filled sac through a dysraphic defect in the upper cervical spine. So this is the meningocele component. So this is like a cyst within a cyst and the outer cyst is the meningocele. And the inner cystic component which is contiguous with the spinal cord is the myelocystocele component. So I find this chart very useful which classifies the neural tube defects. And the neural tube defects can involve the cranium as well as the spine, but we are focusing on spine right now. So spinal defects can be open or closed. Open defects are associated with Kiari malformation and ventricle or megli. While closed defects are not usually associated with intracranial findings. The two open neural tube defects which you need to remember is the myelomeningocele which is by far the most common and the second is myeloskeesis or myelocile. The most important closed neural tube defect which we'll present with the skin covers a butaneous mass with lipomyelomeningocele and then you have the less common myelocystocele like we saw in this case. So whenever you are evaluating someone with a neural tube defect the first step is to identify whether it's a closed or open defect and that will completely change your differential diagnosis. This is an example of myelomyelomeningocele where you don't have a cystic structure but you have a lipoma which is contiguous between the, between, you have a lipoma along the distance spinal cord and it's contiguous with this subcutaneous fat and again this is a skin cover defect. So this is an example of a fetal MRI with myelomeningocele. So these are fetal, this fetal MRI was obtained at 22 week of gestation and this was obtained at 25 week gestation after in-utero repair of the myelomeningocele. So on the initial MRI we see this large dystrophic defect in the lumbosacral region with a large cystic structure compatible with myelomeningocele. And then intracranially we see findings of KRE2 malformation including a facement of supran infratentorial CSF spaces, small and crowded posterior fossa as well as ventricular megaly. In-utero repair was done sometime around 25 weeks and a follow-up scan four weeks later showed marked improvement in the intracranial findings. Here we can see that the defect has been patched off and intracranially there is restoration of the supran infratentorial extra axial space and marked improvement in the posterior fossa structures. We can again see the system of magna and the basal systems as well as the fourth ventricle appears normal in size. There may be some dysplastic cerebellar tissue but no herniation or crowding at the foremen magna. So myelomeningocele is open spinal dystrophism. It's characterized by a low-length spinal cord which ends in a neural placode and the neural placode extends beyond the level of the skin surface which causes expansion of the associated subarachnoid spaces. Intracranially it's associated with Kiari II malformation and ventricular megaly like we saw in this case. In the recent year our institution has done a lot of in-utero repairs of myelomeningocele and the data on that has been very encouraging. So the initial trial which established the efficacy of in-utero myelomeningocele repair was done in 2011, the MOMS trial. And it showed that in-utero repair either reversed or corrected hindbrain herniation and it reduced the need for v-patient as well as improved the motor outcomes on follow-up exams. The trial was so successful that it has to be stopped midway so that the treatment can be offered to all the patients. Currently in-utero repair can be done either by open approach or a fetoscopic approach and the repair would be just like a postnatal repair when it involves dissection of the neural placode with primary closure of the dura and the skin. There is a grading system for Kiari II malformation which we use to follow-up these patients with in-utero repair. So grade one is normal posterior fossa so you can see the Cisterna magna normal size fourth ventricle and no effacement of the basal system. Grade two is where there is effacement of the fourth ventricle but the Cisterna magna is still preserved. Grade three is the most severe where there is effacement of the fourth ventricle as well as effacement of the Cisterna magna and crowding at the forearm and magnum. So in our case the patient initially had a grade three Kiari II which improved to grade one on the follow-up exam. So in summary, brain malformations, I didn't even attempt to classify them because it's very difficult. One of the reasons it's difficult is because a lot of brain structures develop at the same time so any insult affects multiple different pathways. So the anomalies are associated with each other and it can vary greatly from patient to patient and even identical twins with the same genetic defect, the malformations may look very different. Broadly you can classify anomalies of brain into anomalies of dorsal prosencephalon development which will include anomalies of cerebral commissures like you saw abnormal development of a corpus callosum or malformations of cortical development. Or you will have anomalies of posterior prosencephalon development which will include things like holoprosencephaly and some midline anomalies. You can have anomalies of midbrain or hindbrain development which would include dandy walker syndrome and cerebellar and brain stem hyperblazer syndrome. Or you could have anomalies of the mesenchyme which would be one example would be a cephalosil. Spine malformations again can be classified based on embryology so anomalies of nebulation are the most common with non disjunctions leading to dysrephism. You could have anomalies of caudal cell mass which includes tight phylum and caudal regression syndrome or you could have anomalies of the notocard itself such as split cord malformations. Thank you for your attention. Thank you sir. Thank you for such a wonderful lecture. Dr. Alok Jaajul also be joining us in the main conference. I think his lecture is on the 29th of October that is the second day of our conference so please tune in. I have put the program and the registration link in the chat box so please do register. Our next lecture will be taken by Dr. Manjari Dhege. She is a pediatric and fetal radiologist at the University of Washington. Her topic for today is fetal MRI. Hello everyone. My name is Manjari Dhege. I'm a professor at the University of Washington and I would like to talk about fetal MRI, I would like to thank the organizers for inviting me to give this lecture. So we move on. So fetal MRI was described in 1983. We used low fetal spent magnets but now with the advances that have happened in the hardware and software it's become pretty fast to acquire the images. So we acquire in milliseconds and effectively freezing the movement. So this just shows a number of exams that were done and even until 2000 you can see that the number of MRIs has been progressively increasing over the years and it's gone much more recently as well. So we need to remember that MRI is an adjunct to ultrasound. Ultrasonic is the primary screening modality but we know there are quite a number of limitations with ultrasound. This is what some of these are like reverberation artifact, poor penetration from a ossified skull. When the fetus is, when the mother has oligohydramonous, it becomes very difficult to see fetal structures because of lack of fluid. And if the fetal position is such that you cannot see some of the structures, particularly in late pregnancy. And then some of the abnormalities, especially intracranial CNS abnormalities have not specific appearance on ultrasound. So what are the advantages of fetal MRI? You have superior contrast resignation. You can see if the cranial structure is much better because you don't have the same limitations as ultrasound. You also get a big field of view. And you can do multi-clanar imaging. And of course, the fact that it uses non-ironizing radiation is very helpful as well. So why do we call it as an adjunct to ultrasound? Because we use it a lot of times to confirm the diagnosis or have an alternative diagnosis. We found some additional abnormalities with field MRI as well. And then it's very helpful in patient counseling and pregnancy management. But especially when the providers, when the pediatricians look at these images, it's easier for them to understand MR than to understand ultrasound. And in some cases, it's a problem solver as well. So scan TOS et al. that these guys in 2010 evaluated the combined use of ultrasound and MR for detecting abnormalities. We found that mostly abnormalities of the central nervous system in about 38% of times and lung and thoracic abnormalities where we did fetal MRs. And in 42%, the referral diagnosis was concordant with the post-referral diagnosis after an MR was done. But in 29%, the post-referral diagnosis changed completely. And they found additional findings in almost 28% of the cases. So you take the 29% and 28% together. That's a pretty big number. So this is a case in point. This fetus came to us pretty late, approximately 32 weeks of gestation. And what they had was just mild hydrocephalosmetriculum medley. And it was really mild, but it was very difficult to see the intracranial structures because the color is quite ossified. So we decided to do an MRI in this patient. And then we did the MR, and only we did be fine, the absence of corpus callosum. But you can see that there's a small segment here with this communication between the ventricular system and arachnoid space. And this was a small area of schizencephaly that we found on the MR as well. Another case in point where you have cross sections through the chest in this fetus. The fetus was actually referred to us for pericardial effusion and a normal axis of the heart. So we saw this, we saw the pericardial effusion. But in addition to that, we saw that this doesn't look right. There is an abnormal cardiac axis, but there must be something that is either pushing it or this hypoplasia of the lung on this side. So we decided to do an MRI. And on the MR, what we found was this patient, this fetus, I don't know, right-sided diaphragmatic hernia. You can see the heart is pushed off to the left. The lung is up in the chest. Some of the bowel loops is well up in the chest. And coronal images show you that abnormality quite well. So this was completely misdiagnosed as a pericardial effusion on the ultrasound. But actually it was much more than that. This was a diaphragmatic hernia. This is a postnatal radiograph of that baby. And that confirmed the findings that we had on the MRI. So there are some prerequisites for fetal MR. Usually we use a 1.5 tesla magnet. But in some centers, it started using tesla as well. We use a surface-to-recoil. And we try to do the MR after 18 weeks, both because of the possibility of the magnetic fields interfering with your organogenesis. But also more importantly, because before 18 weeks, structures are really small and it's very difficult to see things on MR. It is important that we get informed consent. We have to make sure that there are no other contraindications for MR, you know, hardware, et cetera, et cetera. We always like to have a recent ultrasound. If the patient doesn't have an ultrasound, we try to get it done on the same day because reading the ultrasound, MRI with the ultrasound is very helpful. So buying possession with feet first, that way the patients are very comfortable. They can look up and out of the magnet if they feel claustrophobic. And we try in later gestation, you know, you try to make the patient with the more mass comfortable as possible. So if they want to be in a left-back to the given disposition to avoid compression of the IVC, we sometimes organize that as well. So we, after doing the localizer with the T2-weighted sequence, we do use a T2-weighted sequence of amnestepathy, a quick look at the, you know, as a localizer to see where the fetus is. And based on that, then we plan our single-shot images. And we try to make it so that they are an orthogonal plane to the fetus. And this is important concept for the technologists to understand that the orthogonal plane in the fetus may be oblique in the model, as a fetus may be in an oblique position. So it has to be orthogonal to the fetus and not to the model. So we, after getting the three orthogonal planes in T2-weighted sequences, we get a T1-weighted sequence as a quick look for any kind of hemorrhage or other bright structures, fat, et cetera. We sometimes get diffusion-weighted images. As a protocol, we get diffusion-weighted images for our brain anomalies. Some of these other sequences are optional. It depends on the time. It depends on how easy is it to get. You know, if the fetus is moving around, it's very difficult to get all the other sequences. We don't give any contrast because it's considered as a category. It's a field drug and has been shown to cause development delay in rats and rabbits. So once the single-shot sequences are done, they take about 18 to 20 seconds. We do some balanced FFP sequences as well. Again, they take about 8 to 10 seconds. And the thing that we are worried about is motion, obviously, and the two types of motion. The maternal breathing motion. So we need to make sure that we get breath-hold sequences. And then feeding motion, which can be bulk motion, where the baby is moving around, baby just flipping, et cetera. Extremity motion, where they're just moving their limbs. And then the fetus is soloing and breathing as well. And that can cause problems with imaging the fetus as well. So what are the indications that we use it for? So we use it for all of these indications, most commonly for CNS and chest abnormalities, mostly diaphragmatic hernia, but we've used it also for neck masses, renal abnormalities, synchrocoxidilteratomas, very helpful in conjoined twins, and then in some cases in twin-twin transfusion as well. So for CNS, EOS, fetal MRI is very helpful, particularly for etiology of ventricleomegaly or posterior fossil abnormalities, and then evaluation of myelination and migration along abnormalities as well. So Deborah Levine from Brigham, she looked at this fetal MRI and found that in about 40% of her cases, MRI led to a change in diagnosis. Twickler also looked at fetal MRI cases specifically for CNS and found that you could see additional information in 64% and change in diagnosis in 28%. But also there was an alteration in the timing or mode of delivery in about 11% of cases. It is important to remember that the fetal brain undergoes development as we go through the gestational ages, so you have increasing circulation and curation as you go into the later gestational ages, and it's important to understand and keep in mind what the brain pattern looks like at these different gestational ages. So these are some cases that I'd like to share. This is a patient who came in with severe hydrocephalus, as you can see in the ultrasound images. I did an LR on this patient and found that it was definitely severe hydrocephalus blown out, ventricle on one side. But the posterior fossil was normal and the third ventricle looked small in size. So this was a patient with epistemosis. This is a patient again was presented for hydrocephalus. The posterior fossil looked normal and then MRI should confirm the hydrocephalus and show that this was again a case of epistemosis. These are two patients. They both presented for increased cisterna magna and you can see that the brain on MRI seems normal except for and the posterior fossil looked normal as well except for increasing the size of the cisterna magna. So this was the cases of mega cisterna magna. Conversely, when you have cerebellar abnormalities and wormian abnormalities, you're looking at that evocomal formation as can be seen in this patient where there's complete absence of the wormis and one of the cerebellar hemispheres appear small in size as well. If you're a woman, hyperglacial would be similar except the wormis would be small in size could actually see the wormis over here. There are measurements that are available that people can do to confirm the size of the wormis on sagittal images and also MRI can help in looking for other abnormalities in these fetuses. This is a patient who had an encephaloseal that was seen on ultrasound and the question was was there anything inside this particular encephaloseal and you could see that there's no brain pattern chimera within this encephaloseal though the intraparent inter the pattern chimera within the skull was dysplastic and disorganized but there was nothing protruding outside. This is a patient who had concocephalitis to be seen on the ultrasound but the posterior phosolope is normal as well and there was this communication between the four-dimensional and the cisterna magna. So on MR we could confirm the findings that there was absence of fumes of the pellucidin as can be seen in these images here's coronal, it definitely shows the absence and then the posterior phosolope looks abnormal it's enlarged, there's absence of the wormis smaller size of the wormis so this was a severe worm in hyperglacia but in addition this baby also had an arachnoid cyst located in the midline as well. This is a patient who came in with hydrocephalus in later pregnancy, the first time the second time the ultrasound was normal and it seemed as if the posterior phosolope looked quite full, had some echogenic areas within it so we did an MR in this patient and yes there was hydrocephalus but the hydrocephalus was because there was a large tumor in the posterior phosolope that was obstructing the outflow and you can see that there was some herniation of this tumor into the upper spinal canal as well. This baby, we diagnosed it as a posterior phosoceratoma this baby went on, was born and you can see that the MR confirmed the posterior phosolope mass there were some areas of hemorrhage within this particular mass diffusion shows restriction unfortunately this baby passed away and on pathology you can see the pathology here there's a large mass that was invading into the cerebellum and into the midbrain and this was a medulloblastoma that this baby had. This is a case in point where at 28 weeks this patient came in with hydrocephalus we could see that there was heterogeneity in the corpus in the Croix plexus and the ventricular walls looked echogenic and there was ventricular megaloma. So we did suspect that either this is a mass or there's hemorrhage within this ventricle so we got an MR done it showed the ventricular megalomagaly the heterogeneity that we saw and then on t even weighted images you could see the blood within the ventricle so this confirmed our findings that this was all blood located within the ventricle and further investigation it was found out that this was non-allioimmune thrombocytopenia causing intercranial hemorrhage and ventricular megalomagaly in this particular baby. These are some postnatal images in the same fetus and you could see similar findings that we saw on the prenatal ultrasound and prenatal MRI as well. So in terms of spine Griffiths found that there was 80% of cases had concordance with ultrasound but 20% of cases had change in management this is a case in point where there is a cystic mass at the sacral end and this you know in these cases what we're looking for is there any inter-abdominal extension of this cystic lesion this is a cystic sacrocoxidium teratoma there was some amount of extension intra-abdominally so it was a mixed intra and extra-abdominal sacrocoxidium teratoma in this one in the baby this was a patient who had an ecogenic mass in the spine there was some vascularity to this ecogenic mass we did an MRI you could normalize the mask it did contain fat within it and so we thought this was a spinal lifeoma this baby actually did get postnatal MR done and you can see the extent of this lesion this was a spinal lifeoma that was confirmed and this was seen on the prenatal ultrasound and MR quite well now face and neck abnormalities is an important important indication we think that because what we do in these patients is sometimes you have to do exit procedure which is the exuterof intra-abdom therapy where the baby is delivered but left on placenta circulation and then once the early is established then the placenta connection is severed so we think that these MRI definitely helps in sort of planning out delivery or method of delivery in these patients you can see the swallowing in these babies you can see the normal location of the tongue and it is very well defined on MRI it's not well defined on ultrasound because of the shadowing from surrounding bones so this is a patient who had polyhydramidias so the baby wasn't swallowing and there seemed to be fullness in the inferior in the in the area inferior to the chin and the anterior neck but it was difficult to define one because of the fluid and because of the shadowing from surrounding structures but when we did an MRI we easily see that there is a large mass located in this floor of the mouth which was obstructing the swallowing, obstructing the airway and also the esophagus and so that's why this baby wasn't swallowing and this was a teratoma in the floor of the mouth another case of point where this baby had severe myocardia as you can see and there's polyhydramidias so we knew that this was a problem this is severe myocardia this baby would need some sort of support in terms of intubation but the real thing the real utility of MRI was in finding out that in addition to the severe myocardia there was retrognathia and the tongue was located quite posterior and it was obstructing the oral pharynx and the nasal pharynx so intubation in this baby through the nasal passages or oral passages would be quite difficult and we could warn the pediatric surgeons that this needed a treat to be performed so that's how we could help in managing the patient and managing the delivery in this patient we find this to be very helpful in teratomas to again localize the airway and see if the airway is obstructed look at the size of the mass and the extent of involvement in terms of non-CNS anomalies as I said diaphragmatic coronia is very important but we've used it for lung hyperplasia and other chest masses as well lungs have different signal intensity at different gestational ages 19 weeks compared to 33 weeks they get brighter and as compared to earlier gestations as well there are papers that have looked at normal and hyperplastic fetal lungs and volumetric assessment this is a good paper from radiology that looks at observed versus predicted volume they could find out that if it was 40% of below the expected then most of the fetuses did not survive the way they did this was they measured the volume ROI around each lung and then added it up and then had a formula for the predicted volume and that's how they could calculate as to what was the difference Kuwashima has looked at signal intensity and they found that the signal intensity ratio between the lung and the liver was less than 2 which are these black circles they had either neonatal death, neonatal death in these patients or really severe pulmonary hyperplasia so in terms of diaphragmatic colonia ultrasound can help and in screening you can see the stomach being up in the chest but MR really shows you the extent of the defect and the structures that are located in addition to locating the residual lung on the other side. This is another patient who has stomach that's located centrally but you could see the lung and calculate the amount of lung that is remaining which can help in post-natal prediction of survival we've so in terms of gastro spaces or other abnormalities like on phallus yields we don't think it is as helpful they may help in sort of if there is a question or if it's a multiple anomaly and this is an incident this is an additional finding that is found but we found in terms of this particular case with MRI to be very helpful this patient had a stomach that was located centrally more central than what we would say is normal and so we decided to do an MR and what we found on MR was you could see the stomach but on the T2 weighted images all the small bowel loops were located on one side and on the T1 weighted images because the large bowel loops are bright because of myconium within them they were all located on one side so we gave a diagnosis of bowel bowel rotation unfortunately this baby did not survive because of other anomalies that this baby had and pathology confirmed our diagnosis where you could see all the large small bowel on one side and all the large bowel on one side and this was a case of bowel bowel rotation other chest masses like sequestration again looking at the extent and looking at the residual lung it's helpful but you can also find other anomalies for example in this patient we found the sequestration you could see the sequestration though but in addition the stomach and the bowel loop seemed to be up in the chest as well and this was sequestration with a CDH as I said it can be helpful in twins especially to look at the membrane if it is very difficult to see it but more importantly in conjoined twins because they are trying to figure out what are the things that are connected and what's belonging where so this is a conjoined twin we can see the connection from the chest down to the pelvis and we could figure out on MRI as to what structures were conjoined that share and what structures were located individually so we do MRI in all our conjoined twins MRI is very helpful in tumors this patient had a normal second trimester ultrasound came back and the third trimester had this big mass very vascular we did an MRI to look at the extent map of the location in addition to the involvement of the structures it was located mainly in the left lobe of the liver and this patient had a postnatal Ct which showed that this was a hematoma in the tibiuma other cases like orthogripposis MRI can help because ultrasound gives you a sense of the finding so I can see the the head and the neck over here I can see on 3D some of the structures but because of its multiple r capability MRI can give you an overall view in addition to looking at specific structures like intracranial abnormalities if there are any there are new advances that people have come out with including all of these so 3D MRI can be done with either T1 or T2 weighted images and you can use it to look at these structures this is more of a research thing and not done as a routine so this particular people in applied radiology looked at bowel and they could see gastrointestinal duplication cysts causing narrowing of the bowel on their 3D images cardiac MR has been done as a research mainly they use multiple untriggered T2 weighted T2 based images you can see a full chamber heart over here similarly here's a baby that you can see the aortic outflow and the doctor lot so again done as a research and not done as routine because I think ultrasound does really well in those cases diffusion rated images can be applied they can be pretty quick and very important for hypoxic ischemic lesions in the brain so we use it as a routine for our CLS anomalies imaging can be both wrong and we've done this as a research study and we've characterized the fetal intracranial brain connections with tractography to assess the structural changes during development so in conclusion it's a useful adjunct to ultrasound very helpful for CNS and chest abnormalities can be a problem solver in abdominal pelvic lesions and very helpful in surgical planning it also increases the diagnostic confidence and as I said the pediatric specialists have experience in reading MR examinations but they have limited ability to interpret sonograms so it's very helpful for them to consult the patient as well thank you very much thank you so much ma'am taking over next we have Matusha ma'am she'll be taking the quiz and so the format is that there are 10 questions the first 8 questions are of course just fun the last 2 questions the winners of the last 2 questions the first 2 people to get to the first person to get the answer right in each question will get a free registration ultimately you can use the registration link that I have posted in the chat box along with the program and we also have paper and poster submissions the deadline is 22nd October which is the next Sunday ma'am if we can start the quiz yeah Bishik am I audible yes ma'am I'll just start the presentation so as Bishik explained we are going to have this short quiz it will be 10 questions and you have to directly put your answers in the chat box the last 2 will be the prize winning questions and the person who gives the correct answer first they get a free registration to the complete 5 day MRI teaching course online edition which we have been talking about so I think we can start with the first question on your screen yeah Bishik you can project it so this is around 11 year old kid who came with frequent episodes of vomiting and this is the MRI so what do you think it is just put your answer in the chat box yeah so I can see people coming up with medioloblastoma appendiomoma ATRT so we can have the answers Bishik in the next slide so this is a case of medioloblastoma the appearance is little different from what we usually expect but a midline tumor in pediatric age group and histopath also came out to be medioloblastoma itself let's move to the next question here I have put in 4 options also to help you out because it's not like a spotter per say a 39 year old who is immunocompetent came with this swelling which was kind of sub acute and slowly increasing in size such that that area became almost like soft inconsistency and it was like a defect in his skull so you can see there are set of MR images and one CT image also which we have provided so what do you think because there are options that it is easy for you it's quite hyper intense on T2 weighted image and I think most of you are getting it correct it is aspergilloma and not osteosarcoma or not lymphoma you can see that it has almost eroded completely the calvarium in that area it is very dark on T2 and even on the gradient or so on images we are getting these focal hyper intensities which is often a marker of fungal infestations because of the manganese and other heavy metal kind of fungal deposits there so this is aspergilloma and we were also seeing this kind of aspergilloma for the first time in this patient our next question so this is something which you people I know the diagnosis must be very easy for all of you so I can if we can have the diagnosis in the chat box first and then I will ask the main quiz question so what do you think it is it's like an exam spotter very common exam spotter when we are preparing for our practicals correct this is HOD which is hypertrophic olivary degeneration now your question for the quizzes which is the tract which is involved in this phenomena so all of you have identified the correct phenomenon which is hypertrophic olivary degeneration what do you think is the tract involved here yes so Dr. Shubham has given the correct answer as dentator rubro olivary pathway so we can have the next screen of it so that is the pathway which is involved in this hypertrophic olivary degeneration dentator rubro olivary pathway so in this pathway if there is any insult most commonly if there is a vascular insult then we see this phenomenon now this is your next question you have to give the diagnosis for this case in a 60 year old with upper abdominal pain and no history of pancreatitis what do you think this cystic lesion in the pancreas is one answer which we have received is colloid opal cyst so you think it is a colloid opal cyst do you think it is coming from the CBD or is it coming from other duct it is not communicating with the colloid opal cyst maybe the images are not 3D here but it is communicating with the pancreatic duct then what do you think it is so I think we have got the correct answer it is IPMN so this is IPMN from one of the side branches so now let's go to the next question so there are two sets to subset to this particular image one is that what is the abnormality in the right breast and then in the left breast so you can just in short mention right and the diagnosis left breast and the diagnosis and if you have confusion regarding right left you can see the heart so cardiac apex is towards the left breast in that case also the smaller one here is the left breast and the larger one is the right breast so what is the abnormality in the right abnormality in the left breast the right radial fold and left rupture of implant by Dr. Shubham and that is the correct answer so if you see on the right side we are seeing something which is usually expected and it's not like insidious finding it is usually seen on a long standing implant it's just a radial fold whereas the left side what we are seeing is an actual implant rupture so we can have the next slide so there are two kinds of rupture and after implant of implantation of silicone or saline breast implants we usually get a fibrous scar formation around the implant shell and there why implants can have intra-capsular or extra-capsular ruptures and we have different different appearances and pathognomonic features of these kind of ruptures now what is the next question now it's question number 6 and just to remind you last two means question number 9 and 10 will be the prize winning ones what do you think this one is a liver lesion T1 and then post contrast we have given directly in a young patient 27 year old yes so correctly mentioned this is FNH and I think all of you Dr. Shalindra, Dr. Shubham, Deepak Vyas all of you are getting it which is FNH only so central scar which is taking up contrast in the late phases but yes we should have put in T2 weighted images as well because that typically have a T2 hyper intense scar in contrast to fibrolemular carcinoma etc. where the scar is not T2 hyper intense next question question number 7 what is this lesion in this final part we have images of sagittal T2 actual T2 and sagittal T1 post contrast yeah so what do you think it is so astrocytoma is something which we are getting is answers intra medullary astro but if you see it's like more like a larger cystic lesion with a small enhancing component eccentrically placed so we can have the next slide answers like it is hemangioblastoma with a typical appearance of a cyst with a solid enhancing nodule yeah so next slide the question number 8 is very easy and then we move to the prize winning question so I think I should quickly get the answers to this it's a typical appearance of something the diagnosis to it which is an emergency situation so what is this a typical MRI appearance of as correctly mentioned by Dr. Shubham Shailendra and Malik Hora as a variant torsion so this is how we see torsion on MRI it's a large ovary scattered follicles in the periphery the centristoma becomes very hyper intense and then other features so twisted pedicle whirlpool sign kind of an appearance of the twisted pedicle we can have free fluid and patient will give history of acute abdominal pain now be quick in answering because the ninth question is going to be on your screen and the correct answer will get you prize so here it is question number 9 so what do you think it is you have to give a complete diagnosis it's an easy one just identify and give a short but complete diagnosis so yes we have we are like getting answers in the chat box so what do you think it is we won't consider spelling mistake because I understand you are making it fast I think we can give it to Dr. Lakshmi Narayan because it is a transplanted fistula Dr. Malik also answered it correctly but Lakshmi Narayan had mentioned left sided fistula transplanted so wish it we can consider Dr. Lakshmi Narayan okay ma'am and keep so yeah let it be I know problems so we take both Dr. Malik Vohra and Dr. Lakshmi Narayan yeah please we request both of you to share your email IDs and if possible phone numbers on the chat box Dr. Malik Vohra and Dr. Lakshmi Narayan and you have been considered for free registration to the upcoming 5 days MRI teaching course online edition and we hope you definitely take advantage of the information that we have available for you to see. Now the last question on your screen so be quick we can display the last question yeah next slide is the question here it is on your screen set of images in multiple planes all of them are T2 weighted images and they make one diagnosis together what is that so that is the thing here which we are depicting so we can have the next slide yeah so here the winner to this is this question will be Dr. Shubham and please share your mail ID and phone number on the chat box Dr. Shubham and we will register you for the upcoming course and this is a kind of a syndromic situation where we get duplication of uterus, cervix and vagina so uterine didelphus and in this scenario it is right-sided hematocarpus but it can be any side and ipsilateral renal urgenesis is there so obstructed hemivagina that is where that ballooning is there ipsilateral renal anomaly is seen so that is oveera or also known as hurlin-werner fundalus syndrome so thank you all for joining us today for the prelude congratulations to the winners please share your details in the chat box and on Sunday again we will have a prelude session there will be 3 lectures back to back that is going to start at 10 a.m so please do join for the same we have again Dr. Alok Jaju then we have Dr. Raj Kedar for MRI and renal masters and we will have Dr. Rashi Shafla talking about MRI and Kolanju Carcinomas this will be followed by a short quiz so participate in that as well with this I think Abhishek you can end today's prelude session okay I will just show the program


Snake parody clip I did not have an NES when I was a kid, but I went to school with a bunch of other kids who did — one friend of particular named Tim also had a subscription to NintendoPower! He generously bought each issue to school with him, and I'd always flip through and get green with N.V. at all the games I never got to play. In the early years of this channel, I tried to remedy that by going over stuff that I missed completely, like Metal Storm, Powerblade, Return of the Ninja, G.I. Joe, Lo G-Man, mostly side-scrolling platformers like that just because I remember them looking like really cool games in Nintendo Power. Well, here we have Kabuki Quantum Fighter, another side-scrolling action platformer and it's developed by Human Entertainment, who later went on to make some oddball games like SOS and Clock Tower for the Super Nintendo, so this is sure to be a weird one. There's a bit of confusion about the title, however. The box says Kabuki Quantum Fighter, the title screen says Kabuki Quantum Fighter, but Nintendo Power just calls it Quantum Fighter, and this commercial, well… Is that 90s enough for ya? It turns out in Japan, this game is known as Jigoku Gokurakumaru and it was made as a tie-in to the Japanese film, Zip Bang, which evidently has a Kabuki dancer as its main protagonist. Most references to that movie were removed when the game was released elsewhere, but I guess there was no way to remove any of the Kabuki stuff since it's the main character sprite, so they just rolled with it and didn't make any mention of it in the commercial or in Nintendo Power.  What is he? George Corpse Grinder Fisher? It's range is somewhat short, but it's still effective. I think it's better than, say, the punching attack in Shatterhand.  You do pick up alternate weapons at the end of each level, and you can switch to them using the select button, and it's the usual range of stuff like missiles and bombs. I'd rather use the headbanging attack, though. You get three lives and three continues to get through six levels. When you die, you start at the last checkpoint, and when you use a continue, you start at the beginning of the level, no passwords here. Each level takes place inside a computer, and that brings me to the story. In the year 2056, a computer virus has infected the Earth's nuclear defense system, and Colonel Scott O'Connor is chosen to upload his brain and consciousness into the network so he can fight it somehow. Kinda like the hacking in Shadowrun, I guess? It's an experimental procedure that's never been done before, so I guess one of the side effects is, uh, dressing as a kabuki dancer? So there's no way this dude is 25 years old, he's like half that age, come on. Anyway, like all action platformers, you can give your character all sorts of cool abilities and whatever else, but the game is only gonna be as good as the level design, and in Kabuki Quantum Fighter, it's just okay. I guess the word to use is conventional, it's very much what you'd expect from a game like this. That's not necessarily a bad thing, it's just very derivative. Friday Night Arcade pointed out the similarities in the design between this game and Ninja Gaiden 2, and after seeing that, it's pretty hard to ignore. Also similar to Ninja Gaiden 2 is The Difficulty. This game features some of the most annoying difficulty you'll ever see. There's speed imbalances, there's blind jumps, there's the stuff in the background that tricks you. Really, I can't jump on this, but this stuff hurts me?  There's a lot of stuff like that throughout this game, and it's not a deal-breaker, but it is frustrating. But I'm willing to bet that if you're into games like this, then you're prepared to deal with all that stuff anyway.  I also have to mention the boss fights, which are just strange. They're pretty much just one-on-one fights on a confined space, but the enemy AI here is just all over the place. The boss bounces around in every direction with no real pattern, which is frustrating when you're trying to use a close-range melee attack. So yeah, in a lot of ways, Kabuki Quantum Fighter represents your traditional NES action platformer experience. It does just enough to elevate it above describing it as generic, but it's not quite good enough to earn a place in that upper echelon of games like Castlevania or Bionic Commando or Mega Man. Still, there's definitely an audience for games like this, so if you liked stuff like Shatterhand, Return of the Ninja, and that kind of stuff, and you're not looking for anything staggeringly original, then you'll enjoy Kabuki Quantum Fighter. And I want to thank you for watching, and I hope you have a great rest of your day.