 I am Devarti Khurshikar. In this last session of an exciting brain series, Time is Brain, I would be presenting few cases of infarcts in different locations. This was a two-year-old male child who had some amount of deviation of angle of mouth to the left, which was followed by left-sided weakness. This was over a period of two days. The patient was a known case of congenital heart disease. He was diagnosed to have tricuspid atresia antinataly, for which he was operated after birth. In view of these findings, an MRI of the brain was performed. The diffusion-weighted images showed that there was a large wedge-shaped area of restricted diffusion on the left side involving the basal ganglia as well as the frontal and temporal lobes. These were the further images which show restricted diffusion. They were appearing bright on DW images and turning dark on corresponding ADC maps. On GRE images, no blooming was seen within it to suggest hemorrhage. Flare images showed hyper-intense signal in that area. Mild mass effect was also seen with effacement of frontal horn of left lateral ventricle. MRI angiography of the brain showed that there was abrupt cutoff within the left-middle cerebral artery in its mid-M1 segment, rest of the left MCA being not visualized at all. Also, the visualized portion of the left M1 segment was small in caliber as compared to right side. So, this was a non-hemorrhagic acute-subacute left-middle cerebral artery territory, in fact, which was due to the thrombosis of left MCA from its mid-M1 segment. This is a very common finding seen in adults due to atherosclerosis but rare in pediatric age group. So, this is a case of a pediatric stroke due to left MCA, in fact. Pediatric stroke is uncommon and the types of pediatric stroke could be ischemic due to arterial or cerebral venous thrombosis or it could be hemorrhagic due to intracerebral or subarachnoid hemorrhage. The arterial ischemic strokes in pediatric age group are classified and have these specific subtypes. But the most common risk factors are congenital or acquired heart diseases as was seen in our case. They could be hematological and metabolic disorders, vascular disorders, infections or uncommon risk factors. This was a 54-year-old female who came with drowsiness and headache since two days on examination she had of thalmoplasia and her GCS was 8. Amara of the brain showed that there was restricted diffusion in the rostral midbrain as well as in bilateral paramedian thalamai. They were appearing bright on diffusion weighted images and turning dark on corresponding ADC maps. This is the sagittal diffusion weighted images which are showing the restricted diffusion in the paramedian thalamai and rostral midbrain. No blooming was seen to suggest hemorrhage and they appeared hyper intense on flare images. MR angiography of the brain did not show any abnormality so did the MR vinogram. So this was restricted diffusion in paramedian thalamai and rostral midbrain with normal angioin vinography suggestive of an artery of perchuron acute infarct. The differential diagnosis for restricted diffusion in bilateral thalamai could be artery of perchuron infarction, deep venous sinus thrombosis or varni case encephalopathy. So this is also called as a paramedian thalamic syndrome and it is a rare type of posterior circulation infarction. This occurs due to a solitary arterial trunk which is supplying bilaterally. It is very difficult to pick up this artery on MR angiography but these are some images which show that there is a single trunk and it is supplying bilaterally. This is 60 years old male who came with alternating hemiplegia and hemianesthesia since 2-3 days. MR of the brain showed that there was restricted diffusion in the medial medulla bilaterally giving a classical heart shaped appearance. There was no blooming on GRE and the MR angiography was within normal limits. So the restricted diffusion in bilateral medulla is due to the medullary infarcts. It is rare and it has a bad prognosis. The classical appearance on diffusion weighted images is of a heart shaped appearance and it is due to one paramedian artery which is supplying both pyramids. This is another similar case which we had in our department where there was unilateral medial medullary infarct. Here you can see restricted diffusion on the medial medulla on the left side. So it is unilateral. So medial medullary syndrome is also called as the inferior alternating syndrome or degerin syndrome. It is usually due to the occlusion of the small branches from the vertebral artery or proximal basilar artery. It is usually the anterior spinal artery which is involved. The classical triad of ipsilateral hypoglossal nerve involvement, contralateral hemiplegia and contralateral hemianesthesia in addition to the classical restricted diffusion within the medial medulla on MRI gives the diagnosis of medial medullary syndrome. 66 years old male came with atexia dysarthria and vertigo. MRI of the brain showed that there was restricted diffusion within the medulla on left side which was posteriorly and laterally. It appeared hyper intense on flare images. So now this is a case of a lateral medullary syndrome which is also called as the Wallenberg syndrome or posterior inferior cerebellar artery syndrome. It can be associated with vertebral artery dissection or due to thrombosis or embolism of the paica of vertebral artery. It also has a classical triad of symptoms which has a crossed pattern. So there are findings ipsilaterally, contralaterally in association with symptoms due to the involvement of vestibular nucleus. So these triad of symptoms along with the restricted diffusion in the lateral medulla gives you the diagnosis of lateral medullary syndrome. 54 years old male had atexia and swaying to the left side since one or two days it was a known case of hypertension. MRI showed that there was a large wedge shaped area of restricted diffusion within the posterior fossa involving the left cerebellar hemisphere. No blooming was seen to suggest hemorrhage. It was causing mass effect with effacement of fourth ventricle and resultant dilatation of third and bilateral lateral ventricles. The T2 coronal images and the T1 sagittal images show the classical involvement of the inferior cerebellum. So this is a case of a non-hemorrhagic paica territory in fact. 75 years old male came with left sided hemiparesis and homonymous hemianopia. MRI of the brain showed that there was restricted diffusion on the right side within the posterior limb of internal capsule and postrolateral thalamus. So this is an anterior coroidal artery in fact. The anterior coroidal artery has a peculiar distribution and hence gives a classical triad. So it supplies a posterior limb of internal capsule which gives a contralateral hemiparesis. It also supplies a ventral postrolateral nucleus of the thalamus which gives the hemisensory loss and the lateral geniculate body which gives the homonymous hemianopia. The anterior coroidal artery originates from the posterior wall of internal carotid artery, 2 to 5 mm distilled to the origin of PCOM and 2 to 5 mm proximal to the carotid bifurcation. Isolated anterior coroidal artery in fact are rare and they are usually a part of the MCA in fact. You can get the complete triad of symptoms only when it is a large anterior coroidal artery stroke. 26 years old female had a normal vaginal delivery but on 8th postpartum day she developed severe thunderclap headache which was followed by right sided weakness. So an MRI of the brain was done which showed that there were multiple discreet and few confluent areas of restricted diffusion bilaterally. Most of them were in watershed territory areas. They did not show any hemorrhage and on flare they were hyper intense few of them showed mild mass effect. So considering these findings one could think of a embolic or a cardio-embolic stroke. Her MR angiography was very interesting. This is the angiography of the circle of Willis which showed that bilateral internal carotid arteries in their intracranial segments as well as bilateral intracranial vertebral and basilar arteries are good calibred and show good flow. But the bilateral middle cerebral and anterior cerebral arteries are small in calibre and show patchy poor flow. In addition there are multiple short segments of narrowing scene within them bilaterally. Also their peripheral vessels are attenuated. Both posterior cerebral arteries also showed similar findings with multifocal segments of narrowing. The neck vessels showed that there was good flow within the vessels. So this is a stroke mimic which is called as the RCVS or cerebral vasoconstriction syndrome which is reversible. So the classical finding is that the patient presents with a thunderclap headache which is due to the vasospasm of the cerebral vessels and this is reversible. It is more common in females. There are many associated or predisposing conditions such as pregnancy and puperium, exposure to drugs and blood products, high altitude or certain miscellaneous causes. Our case was a postpartum. Initial stages of CT or MRI may be normal but in later on there could be hemorrhages such as convexity, subarachnoid hemorrhage or low bar hemorrhage. There could be infarcts which are there classically in watershed territory areas or there could be only vasogenic edema. There could be findings together, some of them or all of them also. Classically the CSF is normal. Angiography is most important. It could be a CT or an MR angiography or a DSA which shows that there are multifocal narrowing in the circle of villus and its branches. There could be post stenotic dilatations which gives a classical beaded appearance or sausage shaped arteries. A contrast MR angio may sometimes be used if you want to differentiate it from vasculitis in which case you could get enhancement along the vessel walls which are involved.