 Good morning, everyone. I am Dr. Shpali Asati, PSJR group of department of pre-do diagnosis in Mozaffar Medical College and Hospital is presenting paper on the topic, role of MRI brain in evaluation of children and developmental delay. Introduction. Development is a continuous process that begins in vitro and progresses until maturity. This process involves structural and functional stages of progress or growth. Developmental delay is a defined as significant delay in one or more developmental domains of children. The evaluation of childhood developmental delay is essential. As it allows for early diagnosis and treatment and health and counseling periods regarding the outcome of their child and to identify any possible risk of re-organization. Neuroimaging prefabric MRI of the brain should be obtained when specific clinical indicators are present. MRI is an essential tool to diagnose the cause of delayed milestones. MRI aids in visualizing structural abnormalities and ideological causes of delayed milestones. The abnormal neurological primings were seen in 60 to 65% of the cases. The most common cause is hypoxic issue with injury. And the second most crucial structure involved is corpus callus. Structures that are systematically evaluated are ventricles, corpus callus, ventricles, gray and white matoch, besegalia, brain stem, sedimilum. The aims and objectives of my paper are to study the role of MRI in evaluation of child with developmental delay to identify the spectrum of abnormalities in children with developmental delay in MRI brain to characterize the abnormalities based on age, ideological factors and involved brain structures. Methods. This is a descriptive prospective study involving sample of 20 patients of 0 to 10 years who presented a developmental delay and a referred to department of neurodiagnosis. All these patients who were fulfilling the inclusion criteria in our endowed, after proper explanation of the procedure and the purpose of the procedure written informed consent was obtained from the patient. All the children were properly sedated during neuro, before the neuroimaging. The patient were placed in supine position and the head is placed securely in receiver coil. Brain MR images were obtained using CMAR magnitude essence of 1.5 Tesla MR machine using CZ protocol routine sequences were acquired that is actual coruminal, societal T1 T2 flare, DWI, ADC and post contrast T1 weighted sequences. The representative cases, my first case was of one year female child presented of Caesar's and did it right. This T1 weighted and T2 weighted actual scan MRI. There is prominence of the subarachnoid spacer in the bilateral cerebral hemispheres with mild prominence of the bilateral lateral ventricles, the possibility of mild cerebral atrophy with the white matter in the periventricular region and the central semi-oval and there is also, there was thinning of corpus callosum, mainly of sprenum, likely periventricular locomotion. In my second case, this is our three month female child presented with Caesar's in this T1 weighted and T2 weighted scams, T1 and flare sequences in this T1, there is T1 and flare hyper-intensities noted in the bilateral central semi-oval and bilateral coronary data region, likely old ischemic insult. In my case, three is of a nine month male child presented with developmental delay. In this T2 weighted and T1 weighted actual scans, there were multiple, there is multiple linear alternate hypo and hyper-intense bands involved in the white matter predominantly in the bilateral periventricular regions and central semi-oval radiating perpendicularly from periventricular margins demonstrating the differential diagnosis is of metachromatic leukotestrophy. In my case, fourth, this is our four year male child, female child presented with delayed milestones and delayed cry. In this, there was a CSF intensity extra action cyst in the left frontal region, likely adepnoid cyst. In the case, fifth, this is our six month male child presented with Caesar's and developmental delay. This is our T2 weighted and this is a GRE sequence. In this T2 weighted, there is a hyper-intense lesion, well defined hyper-intense lesion in the bilateral basal gallea and in this, there is central GRE hypo-intensity intonation differential diagnosis is a metabolic encephalopathy. In my case, sixth is our three year female child presented with Caesar's and developmental delay. In this T2 weighted flare and T2 sag section, there is symmetrical focal atrophy of the bilateral parietal occipital regions and there is abnormal T2 flare hyper-intensities in bilateral cerebral hemispheres and thinning of corpus callus and sequelae of HIE. In my case, seventh, this is our 1.5 year male child presented with complaints of global developmental delay. In this, the title T2 and T1 weighted sag sections, there is non-visualization of the body and the spinaeum of the corpus callus and likely partial adenesis of the corpus callus. In the same patient, the occipital haunts of the bilateral lateral ventricles were cross diluted, but the anterior haunts body and the temporal haunts of the lateral ventricles are not diluted as well as the third and fourth ventricles were also non-diluted, likely the diagnosis is of corpus epheli. So the observation and results of my paper presentation is, our study involved the evaluation of 20 children of age 0 to 10 years who presented with developmental delay. The study revealed the significant number that is 7 of children presented with developmental delay in age less than 1 year, 4 were there in each 1 to 2 years, 3 to 5, 6 to 8 years and only 1 child was in the age group of 9 to 10 years. The study revealed abnormal MRI findings in significant 6 number of children aged less than 1 year, that is 6 children presented with abnormal MRI findings, 3 children and 2 children in 1 to 2 years and 6 to 8 years each and only 1 child in age group of 9 to 10 years presented with abnormal MRI findings. The MR images were evaluated in detail in regard to various structures involved in our study. The corpus callusum was involved in 35% of the cases, basal ganglia in 15, white matter involvement is of 25% of cases and ventricles in 20% of the cases. This same chart is shown in this. The prevalence of abnormal MRI findings was in 70% of the cases in the evaluated patients, only the 30% patients out of 20 patients were normal. Another discussion of this paper is the developmental delay has multiple entomologies, many of which cannot be diagnosed without the use of neuroimaging, such as the degree of perinatal hypoxic insult and the sexual brain abnormalities. Our studies showed that the prevalence of abnormal MRI findings in the brain were in 70% of the patients and similar prevalence rate has been reported in these following studies. Some of the children with abnormal MRI findings were in the age group of 1 year or less and females were slightly more in number than males. In 14 cases of our study there was abnormal MRI findings and the anatomical structures were evaluated. So conclusion of my study is MRI evaluation of the brain contributes to the diagnosis of etiologies of developmental delay. Clinical diagnosis of the developmental delay should not be the only endpoint. MRI is the best investigation with a high yield in such developmental delay patients. The potential MRI will be necessary to ascertain disease progression. Advances in MRI imaging, that is functional MRI, MRs were proceed team, DTI and spectrography, especially in structural and normal brain of such children should provide more yielding information. These are my references. Thank you.