 Hello, I'm Dr. Balaji, junior resident from MG Medical College in Mumbai, and my topic is Phecomatosis Revisited, a pictorial review. Introduction. Neurocutaneous syndromes or Phecomatosis are a heterogeneous group of congenital disorders, primarily involving structures derived from the embryological neuroectoderm. All of these syndromes involve the central nervous system, peripheral nerves, skin, and other systems. There are about 20 to 30 disorders classified as neurocutaneous syndromes. The aim is to review the role of MRI as a method of imaging to diagnose patients with neurocutaneous syndromes, and the objectives are to illustrate the MRI imaging findings of few common neurocutaneous syndromes and to review imaging and clinical features of common presentation of Phecomatosis. This is a retrospective study done in MG Medical College over a period of six months from June 23 to December 23, and a total of 18 patients were included and always scanned on Toshiba 1.5 Tesla MRI machine. These are the cases. Moving on to the first case, we see multiple areas of flare hyper intense signal involving the sphenium of corpus callosum on the right side, bilateral ganglion capsular regions, midbrain on the right side, peri-ventricular area of ponds. This is a case of focal altered signal intensity in a case of neurofibromotorosis 1. Moving on to the next case, here we see a small rounded relatively well-defined lesion involving likely arising from the medulla of Langata, extending into the left cerebellum medullary system, which appears hyper intense on flare images and shows no restricted diffusion, and on post-contrast study there is no post-contrast enhancement seen. This is a low-grade tumor, likely a low-grade glioma in a case of neurofibromotorosis 1. Moving on, we see multiple variable sized T2 hyper intense lesions extending from the skull base up to the anterior medial synom involving the entire left side of the neck, which shows T2 hyper intensity with central hypo intense areas such as two of plexiform neurofibroma. These show mild to moderate enhancement on post-contrast study. The same patient on sagittal image showed a severe typhotic deformity at the level of C2, C3, C4 and acute angulation at the level of C3 causing spinal canal compression and spinal canal stenosis. The same patient showed multiple T2 hyper intense lesion involving both sides of the ribs along the both sides of the ribs which showed mild to moderate post-contrast enhancement such as two of intercostal neurofibroma and also we see the medial senile extent of the neurofibroma. Moving on to the next case, here we see diffuse thickening of the skin and subcutaneous tissues of the entire foot and the distal aspect of the leg, which shows multiple star hyper intense lesions with hypo intense foci, such as two of plexiform neurofibroma foot in a case of neurofibromatosis band. Moving on to the next case, here we see well-defined extraactual lesion in bilateral cerebellopontane region extending into the internal acoustic meiasis, which suggests two of bilateral acoustic schwannomas in a case of neurofibromatosis II. The next case, here we see there's a cystic lesion with a neural enhancing nodule in the upper half of the spinal cord in the cervical region and also we see there are two hyper enhancing nodules just below the cystic lesion, which is suggestive of amangioblastoma involving the spinal cord in a case of worn hippo-lendocentral. Moving on to the next, this is the same patient in which we saw that there was the bilateral cerebellar hyper enhancing foci, keeping it consistent with cerebellar amangioblastoma in case of worn hippo-lendocentral. The same patient had T2 hyper intense area in the peteras part of the left temporal bone, which showed subtle post contrast enhancement, which is keeping it consistent with endolymphatic sag tumor in a VHL case. Moving on to the next case, here we see that there is a T2 hyper intense lesion involved and flare hyper intense lesion involving the frontal horn of right lateral ventricle. In the case of tuberous sclerosis, this is a diagnostic of subepandymyl gensel astrocytoma. We could also see in the same patient that they were discrete and confluent T2 flare hyper intensities in bilateral frontal and parietal occipital regions, which is suggestive of cortical and sub-cortical tubers in the case of tuberous sclerosis. Moving on to the next case, here we see prominence of the cortical sulci along with enlargement of the subarachnoid space in the T2 image, along with subtle flare hyper intensity along the cortical sulci in left parietal occipital lobes and mild thickening of the ipsilateral chloride plexus. In the inversion recovery image, we can see the volume loss, well appreciated. On post contrast study, there is a serpentine pile enhancement along the cortical sulci and gyri of the left parietal lobes, parietal occipital lobe with thicken and enhancing ipsilateral chloride plexus, suggestive of Sturge Weber syndrome. Moving on to the next case, here we see that there is prominence of the cortical sulci with enlargement of the subarachnoid space, showing pile enhancement along the cortical sulci and gyri of the right frontal parietal lobes, suggestive of right sided hemiatrophy with pile and gematosis in the case of Sturge Weber syndrome. In the next case, we see that there is a left sided hemiatrophy along with the T1, T2 flare hypo intense signal along the left parietal occipital lobes, which shows blooming on GRE, suggestive of calcification. On post contrast study, we see that there is a pile enhancement along the cortical sulci and gyri of the left parietal occipital lobe with thickened and enhanced chloride plexus, suggestive of Sturge Weber syndrome, again with calcification. So, the brief discussion, these are the common neurocateness symptoms which we encounter. And so, this is a table summarizing all the salient features of the same. And just to highlight few points, all of these neurocateness symptoms which are illustrated so far is an autosomal dominant inheritance, apart from Sturge Weber syndrome, which is sporadic in inheritance. Apart from that, there are multiple cutaneous manifestations of these neurocateness syndrome which plays a major role in diagnostic criteria of the same. And to conclude, Pekomatosis group includes nearly 30 and more individual symptoms. Although genetic testing is available, manifestation of these symptoms cover a wide range. Imaging plays an important role in screening, early identification of abnormalities and follow up of patients in previously diagnosed cases. Radiologists should be familiar with these symptoms to guide appropriate treatment and prognosis. Thank you.