 Good morning everyone, this is Dr. Swami Aranjan from Goa Medical College and today I am presenting a case report on thrombosis of azygous anterior cerebral artery. Introduction. Azygous anterior cerebral artery is a rare variant of the circle of villus where two A1 segments of the anterior cerebral artery will combine to form a single and medium vessel near the origin of the normal anterior communicating artery. The single anterior cerebral artery in the midline serves as the common blood supply to the medial hemispheres. Occlusion of the azygous anterior cerebral artery therefore can cause spice hemispheric and corpus callus infarcts. History. My case is a 68 years old male presented to the emergency room with acute onset of right upper and lower limb weakness as well as slowness of speech for one day. Patient was a known case of hypertension and chronic kidney disease. He was a chronic alcoholic and had stopped four years ago. No history of trauma was noted. No headache, vomiting, fever or decreased urine output noted. On examination, patient was a febrile, a pulse rate of 80 beats per minute and a BP of 160 by 90 mmHg were recorded. The heart sounds were normal and the lungs were clear. The abdomen was soft and non-tender. Neurological examination revealed decreased verbal output. Tone was increased and great zero power was noted in the right upper and lower limbs. Planta reflexes were up going on the right side. Soon after admission, patient developed weakness of the left upper and lower limbs and had one episode of left sided focal tunic seizure. Neurological examination showed increased tone and great zero power in all four limbs. Planta reflexes were up going on both sides. The laboratory data was as follows. The hemoglobin was 13.1 gram per deciliter, hematocrit was 37.2% and a total ecocide count was 4.36 lakhs. Serum creatinine level was 7 mg per deciliter and serum urea level was 119 mg per deciliter. Rest of the laboratory parameters were normal. CT was ordered at the casualty level and picked up cortical atrophy. No other pathology could be identified. Further evaluation with MRI revealed, on T2 weighted images, image A shows hyperintensity involving the bilateral paramedic frontal parietal regions on axial sections. Image B shows hyperintensity seen further involving the corpus callus on coronal sections. Flare sequences show T2 hyperintense lesions appearing hyperintense on flare sequences also. DWIN ADC sequences revealed areas of high signal noted in bilateral frontal parietal regions and the rostrum and genu of the corpus callus with corresponding low signal areas on ADC sequences which are shown in the red arrow. 3D time of flight sequences revealed two A1 segments of the anterior cerebral artery combining to form a single midline vessel near the origin of the normal anterior communicating artery which is not seen to continue into the hyperital region suspicious for thrombosis. Discussion Normally, the anterior cerebral arteries arise from bifurcation of the internal carotid arteries on either side and cross the anterior perforating substance. At this point, they interconnect with the anterior communicating artery. This anomaly resembles the lower privates where there is no anterior communicating artery and A1 segments of both anterior cerebral arteries fuse to form an azycos artery. The anterior communicating artery is absent or hyperplastic in this anomaly. The incidence of this anomaly is approximately 0.3 to 1%. The clinical significance of azygos anterior cerebral artery is the alteration of arterial hemodynamics of the frontal lobe and increased incidence of malformations like agenesis of corpus callusum, heightened calfile, sacular aneurysms or AV malformations. These are my references. Thank you for your time.