 Hello everyone, I am Dr. Shantanu Gupta, junior resident from Tobu Valley National Medical College at BYL Nihar Charity Hospital in Mumbai. Today I am going to present a paper on role of MRI and positive post malformations along with my co-author Dr. Marisha Joshi, assistant professor and under the guidance of Dr. Dave Shetty, professor on HOD. For genetic positive post malformations can result from genetic or disruptive mechanism. Genetic mutations causing malformations make a deal over how can we inherit it from the parents. Evaluation of positive post malformations with significant advances in neuroimaging techniques both pre and post natal have enabled better definition and classification of the same. Here we shall demonstrate few cases in spectrum of positive post malformations where correct differential diagnosis create a paramount importance not only for claim to follow-up and prognosis of patient but also to appropriately counsel the families for inheritance. Thus for each disorder we shall emphasize on key neuroimaging findings that were needed for the diagnosis. The aim of this study is to evaluate the role of MRI in detecting positive post malformations. The study was conducted in the department of neurodiagnosis, TNMC, Mumbai. The study was carried out using MR Flicks Achiever scanner which possesses a superconducting magnet of 1.5 tesla strength. The study included precise from people of pediatric age group who represented developmental delay, neurological symptoms like difficulty swallowing, balance problems, amniolibomins and cranial nerve abnormalities. Diagnosis was based made on typical MRI appearances, location and associated features. The first case is of a one month old female infant born of a sanglass marriage. The child presented with complaints of inability to suck milk since birth, multiple episodes of GTCS. Who are responsible to suck and react reflexes suggestive of period of abduction. The patient died after two months after multiple episodes of aspiration demolition. On MRI imaging T2 erasal images revealed molar tooth like appearance and T1 inversion recovery images revealed hypoplastic middle cerebellum peduncle. The mid suggested T1 images revealed flattening of ventral pons along with narrowing of dorsal ventral mesas well extremus and dorsal pontile tigmental cap. DTI images revealed atopic pontine transverse fibres as shown with standard diffusion DTI is superimposed color coded fractional anisotropy images showed tigmental cap, bundles of transversely oriented fibres representing atopic pontine transverse fibres. The amazing features of the molar tooth like configuration of quantum mesensival ejection, dorsal pontine tigmental cap and presence of atopic transverse pontine fibres well demonstrated on DTI in even the accurate diagnosis of pontine tigmental cap dysplasia, ETCD. Now what is the difference between JS as yogurt syndrome related disorder and PTCD? Genetically PTCD genetic basis yet to be determined by JSIDs autosomally recessive. Molar tooth sen can be seen in both, pontine tigmental cap is not seen in JSID but can be seen in PTCD always. Clinical features include of JSID, retinopathy, congenitripetic fibrosis and polydactyl. PTCD can present as multiple cranial neuropathies, vertebral and rib anomalies. Prognosis of JSID varies based on multiromeral involvement. In PTCD, cranial nerve palsy is usually improved with age, however death occurs due to aspiration pneumonitis as early as one month. The second case is of our four-year-old female child presenting in hypotonia, post facial features, global developmental delay and extraprimandal features. mRNA mailing revealed on T2XL images, thinned and elongated posterior cerebellar peduncle with deepened interpenicular forces. On T1 inversion recovery, we could see subparticle white matter showing multiple discrete areas of gray matter and nodular areas in perimentopolar areas as gray matter atotopyla. Intensory imaging showed horizontal orientation of superior cerebellar peduncle. Our diagnosis was Dover syndrome, also known as women hyperplasia or molar tooth in mid-brain high and mid-mel formation. The following case had been detected during routine ultrasound anomaly scan and was sent for fetal MRI for further evaluation. Fetal MRI showed large intramaspherexists and women eplasia with prominent osteo-interpenicular forces. After birth, the child was brought for a full-up scan, which showed women eplasia leading to stressed appearance of superior cerebellar peduncle, giving a molar tooth-like appearance. There was also cystic dilation of fourth ventricle and extending posteriorly along with occipital meningocell. There was also well-defined large in unilocular anterior intramaspherexists along with polymicrovaria and right ventral cortex. Our diagnosis was dendipocrine continuum with Dover syndrome, signs and symptoms of the same include peak muscle tone, abnormal breathing patterns, abnormal eye movement, a texid. Displazion and heteropeas are common. The following case was a seven-month-old male-presenting with the best care reflex, involuntary reputed downward eye movement with loss of consciousness and swelling in lower back. A USG of swelling revealed a mild meningocean. On MR imaging, T1 sagimage showed descent of cerebellar tonsil in the cervical canal and effacement of retro cerebellar CSS. Lumbar spine sequences showed a spinal defect with associated mild meningocean. Our diagnosis was an unknown carry type 2 menformation, which is characterized by mild meningocean, a small posterior fossa, with descent of brainstem, cerebellar tonsil and vermice through form and magnum. Imaging differences include spinal astrocytoma, care even venformation, cordon. The next case is a 11-year-old female who came with complaining of headache and fever since four days. She had been experiencing aggravating neck pain during exercise for two years. T1 sagimage showed perillac cerebellar tonsil and radiation along with crowding of form and magnum and effacement of free medullary and cerebellar medullary system was noted. Cervical spine MR showed long segment settings in spinal cord extrusion from lower level of C2 to lower level of D2 along with retroflexion of dense. There was also fusion of C1 and C2 vertebrae in the posterior spine. Our diagnosis was an unknown carried menformation 1.5. Since cerebellar tonsil descent was 9mm and descent of hopex was noted by 4mm below the level of form and magnum, they were also associated with syringomylia and bone aorticis. In conclusion, we can say the neuroimaging used detailed anaerobic findings and plays a key role in diagnosis of congenital positive musam inflammation. Thus prenatal diagnosis of Joer syndrome has proven difficult because of relatively non-specific prenatal ultrasound findings reported in most affected fetuses. A further limitation of prenatal ultrasound is the difficulty in obtaining sedatal views due to fetal orientation. Advantages of MRI or ultrasound include superior tissue discrimination and resolution, elimination of ultrasound artifacts and ability to achieve multiple planes of imaging including sedatal views, regardless of fetal position. A developing carrier can limit ultrasound visualization of the brain but does not hinder visualization by MRI. Diffusion Tensile Imaging is a promising method for characterizing microstructural changes or differences with neuropathology. Overall, TTI enhances the ability to diagnose PTCT by providing detailed information about microstructure of white matter tracks in the brain, allowing for better visualization and characterization of abnormalities such as those in PTCT. These are my references. Thank you.