Radiologists refer to any area of cerebral parenchymal loss with or without surrounding gliosis as encephalomalacia. This archaic phrase, which literally translates to "softening of the brain" due to liquefactive necrosis, was coined by pathologists to describe the macroscopic appearance of the brain following a variety of traumas, such as cerebral infarction. The final outcome of brain parenchymal liquefactive necrosis after insult, which typically happens after cerebral ischemia, cerebral infection, hemorrhage, traumatic brain damage, surgery, or other insults. Gliosis, or the growth of glial cells in reaction to injury, is frequently seen around it. The location, size, and number of the lesions as well as the existence of other issues like seizures, hydrocephalus, or infection affect the symptoms and prognosis of encephalomalacia. While some people might not have any symptoms, others might have neurological abnormalities such hemiparesis, aphasia, cognitive decline, or behavioral changes. Depending on the underlying reason and the severity of the problem, treatment options may include medication, surgery, or rehabilitation. This is a case of a young male who reported for rehabilitation his left upper limb weakness, upon investigations Encephalomalacia was diagnosed.

Moyamoya disease is also termed a spontaneous obstruction of the arteries in the circle of Willis. It is recognized as the leading cause of ischemic and hemorrhagic stroke. The infrequent cause of stroke is radiologically characterized by the continuous progression of stenosis of the end portion of the bilateral internal carotid artery and compensatory capillaries collaterals. A 1yr old child was admitted to the pediatric I.C.U with a complaint of decreased sensorium, decreased food intake and decreased right upper and lower extremity movements past two days. He had a history of convulsions at seven months of age. He was diagnosed with Moyamoya disease on Magnetic Resonance cerebral angiography. The clinical findings on MR-Angiography show multiple collaterals noted around Circle of Willis, specifically around the posterior communicating artery, anterior communicating artery, posterior cerebral artery, bilateral lenticulostriate, thalamoperforating arteries and medialfrontobasal arteries, which is suggestive of Moyamoya disease. Magnetic resonance imaging of the brain shows Gyral diffusion restriction in a right fronto-parieto-temporal region with mild swelling. The above clinical findings on MR-angiography show the Moyamoya disease in 1year old male child. These clinical findings on MR-Angiography and M.R.I – brain and neck can help the clinician accurately diagnose and manage this rare case.

Edward syndrome, clinically known as trisomy 18 syndrome, is an autosomal chromosomal disorder characterized by an extra copy of chromosome 18. It belongs to the category of autosomal trisomy syndromes and is the second most common, with trisomy 21 being the only more frequent occurrence. In the context of this research, we present a case study focusing on a 3-month-old female infant admitted to the emergency department due to a complex array of symptoms. The primary clinical manifestations included a persistent cough, cold, and fever lasting for eight consecutive days. Comprehensive clinical evaluations, encompassing radiological and hematological investigations, confirmed the diagnosis of bronchiolitis along with viral bronchopneumonia. Chest X-rays revealed bilateral patchy opacities and diffuse haziness, primarily concentrated in the right hemithorax. Beyond respiratory issues, the infant displayed a range of distinctive physical attributes, including low-set ears, micrognathia, cranial anomalies, flattened nasal bridge, widely spaced nipples, overlapping fingers, abdominal distention, rocker-bottom feet, and recurring limb deformities known as recurvatum. Attempts to correct the limb deformity with a hip spica cast over an extended month-long period proved unsuccessful. Chronic villus sampling (CVS) ultimately confirmed the presence of Edward Syndrome (Trisomy 18), linked to the extra chromosome 18, leading to diverse physiological and developmental abnormalities. This case underscores the critical importance of timely and precise diagnosis, highlighting the challenges involved in addressing complex medical conditions marked by multifaceted clinical phenotypes.

The term "Osmotic Demyelination Syndrome" (ODS) is synonymous with central pontine myelinolysis (CPM), denoting a condition characterized by brain damage, particularly affecting the white matter tracts of the pontine region. This damage arises due to rapid correction of metabolic imbalances, primarily cases of hyponatremia. Noteworthy triggers encompass severe burns, liver transplantations, anorexia nervosa, hyperemesis gravidarum, and hyperglycaemia, all linked to the development of CPM. Clinical manifestations encompass a spectrum of signs and symptoms, including dysphagia, dysarthria, spastic quadriparesis, pseudobulbar paralysis, ataxia, lethargy, tremors, disorientation, catatonia, and, in severe instances, locked-in syndrome and coma. A recent case involving a 45-year-old woman illustrates these complexities. Upon admission to the Medicine Intensive Care Unit, she presented with symptoms indicative of diminished responsiveness and bilateral weakness in upper and lower limbs. Of significance, the patient had a pre-existing medical history of hyperthyroidism. Extensive diagnostic investigations were undertaken, revealing compelling evidence of profound hyponatremia through blood analyses. Furthermore, magnetic resonance imaging (MRI) was performed, unveiling conspicuous areas of abnormal hyperintensity located in the central pons, intriguingly accompanied by spared peripheral regions. These radiological findings align with the characteristic pattern associated with osmotic demyelination syndrome, illuminating the underlying pathology.