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Hyperacute Intrapardnchymal hematoma Rt thalamus with mass effect

71yr,M, Presented with left sided weakness of acute onset about 10 days ago .He also has numbness of left side. For the above complaint he was admitted and evaluated at the local hospital but no relief in the left sided numbness. He denied having any head ache / vertigo / vomiting. Known hypertensive20yrs .Not taking any medicine other than telmisartan and Cilacar. Non smoker,not in the habit of taking ethanol. On exam BP 150/ 90 mmhg. Mold facial asymmetry left side.Partial ptosis rt side.Gr3/ 5 power left side with ,with spasticity and left sided pyramidal signs.He has dulling of all modalities of sensation left half of the body.No bruit over the carotids/ vertebrals. What abnormality I the MRI brain ?

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Thanks Curofy and other doctors. Discussion what abnormality in the MRI brain. MRI brain shows well defind round T2/ FLAIR hyperintensity,isointense to T1w images at the region of thalamus extending to posterior limb of internal capsule,and rt periventricular frontal coronaradiata causing mass effect in the form of mild effacement of body & atrium of rt lateral ventricle. Mild perilesional edema noted. Imp - Hyperacute intraparenchymal hematoma Rt thalamus.

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Thanks Curofy and other doctors. Discussion what abnormality in the MRI brain. MRI brain shows well defind round T2/ FLAIR hyperintensity,isointense to T1w images at the region of thalamus extending to posterior limb of internal capsule,and rt periventricular frontal coronaradiata causing mass effect in the form of mild effacement of body & atrium of rt lateral ventricle. Mild perilesional edema noted. Imp - Hyperacute intraparenchymal hematoma Rt thalamus.

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Ischemic stroke rt thalamic region Cerebral oedema Hydrocephalus follow up mri Opinion of neurologist So left sided effect Midline shift to left

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Intraparenchymal Hemorrhage Related terms: Hematoma Magnetic Resonance Imaging Hypertension Aneurysm Intraventricular Hemorrhage Subdural Hematoma Intracranial Hemorrhage Traumatic Brain Injury Subarachnoid Hemorrhage Arteriovenous Malformation Opening pressure Patients with IPH are more likely to have an elevated OP compared to those with ischemic stroke. Elevated intracranial pressure (ICP) is more likely to occur because of a more sudden increase in intracranial volume from the clot itself compared to the subacute development of edema surrounding a stroke. In one series of 70 patients with autopsy-proven primary IPH, the OP ranged between 30 and 1,100 mm CSF. The OP was greater than 200 mm CSF in 57% of patients, greater than 300 mm CSF 38% of the time, and greater than 400 mm CSF in 19% of individuals.2 In a smaller series of 14 cases of IPH in whom an LP was performed within 4 days of presentation, the OP was normal in 50% of patients, between 200 and 300 mm CSF 15% of the time, and greater than 300 mm CSF in another 35% of individuals.1 Antithrombotic-associated IPH IPH occurs when small penetrating arteries rupture, often in the area of the basal ganglia, thalamus, pons, or cerebellum. The pathology underlying antithrombotic-associated IPH is thought to be similar to spontaneous IPH. The use of antithrombotics exacerbates existing risk factors for IPH. The location of antithrombotic-associated IPH is not different from spontaneous IPH . Cerebral amyloid angiopathy increases in frequency with older age and affects superficial cortical vessels. A prospective case-control study suggests that lobar IPH in elderly patients with warfarin use is often related to underlying cerebral amyloid angiopathy. Similarly, leukoaraiosis has also been shown to increase the risk of IPH in patients taking warfarin following ischemic stroke. Leukoaraiosis was present in 92% of warfarin users with IPH compared to 48% of warfarin users without IPH Hematoma expansion is a risk factor for poor outcome after IPH. Hematoma expansion is thought to result from ongoing bleeding from ruptured vessels, and possibly from additional vessels which are disrupted by the hematoma itself. Coagulopathy may increase the risk of expansion, which is likely to be one of the mechanisms which increases morbidity and mortality.

no contrast MRI.. it could be a bleed, tumor with a bleed

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Subacute rt basal ganglia hemorrhage

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Film show tumor or hemmeroghic infarct N treat accordingly

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Left cerebral heamotoma thalamus

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