 Hello everyone, my name is Oma Prabha, second year junior resident from department of radiology from KVG Medical College, Zulia. Today I'll be talking about multisystem atrophy, rare cell nucleolopathy. So the main objective was to determine the clinical usefulness of MRI imaging in multisystem atrophy through a case scenario. Here's a 66-year-old me who came with history of gait and speech alteration on physical and neurological examination, the findings were as such. The patient had slurred speech, gait atexia and bilateral appendicular cerebellar atexia. Dependent reflexes were present, three or four, and then there was bilateral Bebinski sign positive. Artificial pressure was 130 by 80 mmHg and radial pulse was 60 beats per minute on supine position, and BP was 100 by 70, and the pulse was 70 beats per minute in standing position. So the MRI findings were as such. On axial flare image, we can see the brainstem atrophy predominantly involving the pons in the medulla. Here is a T2-axial image showing diffuse atrophy of cerebellum and the cerebellar pedentals, and T2 hyperintensity involving the white matrax in the pons, giving it a characteristic hot cross bun appearance, suggestive opontocerebellar tract degeneration. We have axial flare T1 sagittal and T2 coronal images of the brain, with the T1 sagittal image showing corpusculosme atrophy, giving it a characteristic double hump camel sign. So I've summarized the MRI findings in this slide. It shows the brainstem atrophy predominantly involving the pons in the medulla, atrophy of cerebellum and the cerebellar pedentals, and T2 hyperintensity involving the white matrax in the pons, and atrophy of corpusculosme. So the impression, diffuse atrophy of cerebellum and the cerebellar pedentals, brainstem atrophy predominantly involving the pons in the medulla, with the hot cross bun sign, features suggestive opontocerebellar tract degeneration. So coming to the topic proper, multisystem atrophy is more rapidly progressive neurodegenerative disorder among the various types of synucleinopathy. The cause of MSA remains unknown, but it can involve the extra pyramidal system, the pyramidal system, the autonomic nervous system and cerebellum. The main clinical manifestations are clear Parkinson's symptoms, a cerebellar ataxia, pyramidal tract signs and autonomic nervous system disorders. Depending on the initial predominant motor deficits, the MSA is subclassified into Parkinson's type, that is MSAP and cerebellar type, that is MSAC. So the conclusion is that it is a rare case of MSAC. MSAC in a 66 year old male with predominant cerebellar signs. Our case is classified as probable MSA since the diagnosis of MSA is defined just with pathological analysis. There is no specific treatment for MSA. Only symptomatic interventions can be made. So these are my references.