 Hello everyone, I am Dr. Pankaj Bundyal, Consultant Radiologist and Director of Bundyal Radiodical Speak Center at Amravati Mahashtra. I have been practicing all imaging modalities since last 21 years, however CT and MRI are my main areas of interest. It is a wonderful feeling to be on Indian Radiology channel. Today, I am speaking on tumor mimics in brain. The condition which mimics tumor are demyelination, inflammatory, infective, that is tuberculosis, fungal or pyogenic, post-treatment, that is post-radiation, vascular malformation, ischemia, arterial and venous, traumatic and degenerative. 20-year-old lady presented with sudden onset of Diplopia with case palsy since 15 days, with history of mild ataxia. Hyper intense signal is seen in pons, almost full pons is involved, no enhancement seen. So no significant expansion, almost entire pons involvement, no enhancement. This is a classical pontine demyelination. Follow-up scan after the treatment shows significant reduction of the hyper intense lesion seen in the pons. Comparison case, a hyper intense signal seen in the pons. The lesion is eccentric in position. Expansion of pons is seen with patchy contrast enhancement. So expansion is eccentric and patchy enhancement. This is a classical pontine glioma. Then we come on case number 2, 16-year-old girl with acute onset of excessive sleepiness for 10 days and history of psychiatric disturbances. Hyper intense signal seen in the region of hypothalamus just adjacent to the third ventricle on T2 weighted images. On coronal flare it is very nicely seen, hyper intense signal in the region of hypothalamus. Post-contrast study shows poor enhancement and follow-up MR treated with IV methylprandisol for 3 days followed by oral steroid, significant improvement in all the symptoms and there is a significant reduction in the hyper intense signal seen in the region of the hypothalamus. So this was a classical hypothalamic demyelination. Then we come on case number 3, low-grade fever, URTI since 5 days with history of convulsions. Multiple hyper intense signal seen on flare and T2 which appears hyper intense on T1. On contrast study open ring like enhancement and the incomplete portion of ring is on the grey matter side of the region. No mass effect, no surrounding edema on diffusion weighted images, mildly increased ADC. MR spectroscopy shows elevation of choline and elevation of lactate. So this was classical TUM effective demyelination. Laps sided severe headache, repeated third nopalcy, single episode of convulsions. An abnormal hyper intense signal seen in the left temporal region on T2 weighted images which appears hyper intense on flare, on administration of the contrast patchy enhancement was seen. So this was classical Rosydafman. It is a idiopathic benign lymphofroliferative disorder mimics lymphoma and other inflammatory conditions on imaging. Lymphadenopathy is also seen, diagnosis based on classical histopath findings. 17 year old boy presented with altered sensorium and history of convulsions. On flare and T2 hyper intense signal seen in the bifrontal region which appears hyper intense on T1 and on administration of the contrast intense enhancement seen along the faults. So this was a classical felsine tuberculosis. Then we come on fungal lesions, history of B cell lymphoma, induction therapy and history of convulsions. MRI shows an iso intense signal on T1 and flare and patchy or punctate hyper intense CT on T2 in the right occipital region. Post contrast MRI shows irregular ring enhancement. On diffusion weighted images and ADC the wall as well as the nodular soft tissue display diffusion restriction while the content don't shows restriction. Single voxel MR spectroscopy over enhancing area demonstrates diminished and acetyl aspartate to creatinine ratio, normal colline to NNA ratio, normal colline to creatinine ratio and diminished myo-inositol to creatinine ratio. So this was a classical fungal lapses. Patient has developed febrile neutropenia, neutrophil count 0, similar lesions in lungs, chest, liver and splem. Succumb to it post-martin confirmed the finding. Case 7 20 year old boy studying in third year of college presented with left sided hemiplegia, lower limb more than upper limb. Hyper intense lesion with hyper intense rim seen on T2 weighted images and on T1 the lesion was hyper intense and rim was hyper intense. After administration of the contrast ring thick walled enhancing lesion was seen. So this was reported as lymphoma or tuberculoma operated outside. Follow-up scan post-op again shows a ring enhancing lesion. This was classical aspergilloma. Aspergillus abscess appear radiologically identical to other brain abscesses as classical ring enhancing lesions with striking high signal intensity on diffusion weighted images. However aspergillus abscess may have peripheral low signal intensity on T2 weighted images. This is better appreciated on GRE or SWI sequences. 50 year old man presented with fever since 5 days left hemiparesis. Abnormal lesion seen in the right parietal region. Mild hyper intense rim on T1 dark to rim due to free radicals, diffusion restriction, peripheral enhancement and lactate peaks on MR spectroscopy. So this was classical pyogenic abscess. Comparison case similar ring like enhancing lesion seen in the right occipital region. Nodularity of the wall is seen. Non-uniform restricted diffusion is regularity of the inner margin on post-contrast scan. In addition to lactate high choline peak was there and on perfusion hyper perfusion of wall was seen. So this was classical necrotic tumor that is GVF. Then we come in to other case. In this we are seeing a hyper intense lesion on T1 with surrounding vasogenic edema in the right thalamus with mild mass effect. Which appears hypo intense on T1 with surrounding hyper intensity. Mild diffusion restriction was seen after administration of the contrast intense enhancement was seen. So this was classical giant conglomerate tuberculoma. Giant conglomerate tuberculoma appears T2 dark, slightly T1 hyper intensity, minimal diffusion abnormality, no GRE susceptibility and intense post-contrast enhancement. This is the other case. In this we are seeing a hyper intense lesion in the right basal ganglia which appears hypo intense on T1. Diffusion restriction was seen but appears hyper intense on ADC. On administration of the contrast heterogeneous enhancement was seen. On MR perfusion it was showing low perfusion and on spectroscopy peak lipid and glutamate seen. So this is a classical intratranial tuberculomas. Comparison case abnormal hyper intense lesion seen in the left basal ganglia which appears hypo intense on T1 with surrounding vasogenic edema. Ring like enhancement seen on the contrast study with mild mass effect in the form of compression of ipsilateral lateral ventricle. MR perfusion shows relatively cerebral blood volume was 2.5. So this was classical metastasis and patient was known case of CA breast. Then case number 9 40 year old men presented with altered sensorium and right hemiplegia. Abnormal lesions were seen in the both cerebral hemispheres of varying sizes with surrounding vasogenic edema throughout the brain. Largest was in the left basal ganglia. On MR spectroscopy reduced NNA mildly increased choline and lactate peak. So this was classical toxoplasmosis. Toxoplasmosis will also show a eccentric dot sign. A ring like lesion with hyper intense rim seen within the ring. Some of the lesion of toxo may be hemorrhagic. So toxoplasmosis it is iso to hypo intense on T1 weighted images. Hettogenously hyper intense with occasionally hypo intense rim that is target sign on T2 weighted images. Variable post contrast enhancement no minimal enhancement no or minimal enhancement to ring or nodular enhancement that is eccentric dot. Hemorrhage occasionally present and MR spectro shows high lipid lactate peak. Lymphoma versus toxoplasmosis. Lymphoma usually periventricular in location while toxo is seen in deep grey structures. No hemorrhage in lymphoma often hemorrhage is seen in toxo. Solitary or multiple lesions in lymphoma always multiple toxoplasmosis. Diffusion restriction with dark ADC values are seen in lymphoma. Usually no restriction if present it is peripheral. High colon or MR spectroscopy in lymphoma only mild increase in colon peak in toxoplasmosis. Now we come on post treatment. 58 year old male operated case of GBM received radiotherapy presented with multiple episodes of seizures and six nerve pulsing. Abnormal expansion region seen in the left occipital region in the white matter extending to the cortex with Swiss pattern of the interior arqueate fibas. MR perfusion shows low cerebral blood volume that is less than one. So this was classical radiation necrosis. Now we come on vascular malformation oblique aneurysms. 45 year old male patient came with sudden onset right plover limb weakness. Well defined hyper intense signal seen in the left frontal region on CT. It appears hyper intense on flare. MR angiography was normal and cavernous malformation are angiographically occult and do not demonstrate arteriovenous shunting. Follow up MRI on T2 and GRE shows blooming. T1 SAGE re and post contrast. Some enhancement is seen on contrast study. So this was classical cavernous angioma cavernous angioma are collection of sinusoidal vascular spaces. Clotted unclotted blood in various stages of oxidation. Slow circulation without a vision ting on MR typical cavernomas looks like raspberry or popcorn appearance. Gradient ecosystem shows this region better than T1 and T2 weighted images. These are the multiple sites of the cavernomas on MRI and CT scan. Now case number 12 35 year old lady presented with headache occasionally tingling in all the limbs vertigo on and off. This is a classical brain capillary telangiectasis. HWI may have high sensitivity equal to GRE in detecting capillary telangiectasis in brain. More often solitary but sometime it may be multiple. Common locations are pons cerebellum or spinal cord. T2 and flare shows normal or slightly increased signal. T1 shows ISO or low signal. T1 contrast study shows tippled enhancement if large can show branching or linear draining veins. So this is classical brain capillary telangiectasis. Case number 13 holocranial headache on and off since three years. Three episodes of TIS in last one year. Weakness of left upper and lower limb with slurring of speech. On examination patient was conscious oriented and no focal neurological deficit. On CT well defined hyper intense signal with surrounding vasogenic edema seen in the right temporal region. On contrast study ring like enhancement was seen but inside the ring there was a intensely enhancing legion seen within the ring. In same study we have done a CT angiography and it was classically a partly thrombosed right MCA aneurysm. It is very nicely seen on CT angiography study. DSA confirms this thrombosed aneurysm. Now we come on in facts and hemorrhages. Case number 14 45 year old male presented with altered sensorium and irrelevant talk. Lower limb weakness came for neurosurgical review. Abnormal hyper intense legion on T2 weighted images seen in the region of corpus callosum. This legion were hyper intense on flare, hyper intense on T1 and diffusion restriction was seen. It was thought to be a corpus callosal lymphoma oblique glioma. But MR angiography was done and there was a narrowing seen in the both sided anterior cerebral artery. So these were bilateral ACA territory in facts. Case number 15 24 year old transplant recipient on triple immunosuppressant presented with left hemiparesis and Diplopia. Abnormal hyper intense signal seen in the right thalamus with surrounding vasogenic edema. On contrast enhancement was seen and on diffusion restriction was seen. On SAGE hyper intense sinuses were seen. So this was on MR angiography. There was a thrombosis of the right transverse sinus and right sigmoid sinus. So this was classical venous in fact. This is the other case in which we are seeing abnormal signal in both thalamus that appears hypo on T1, hyper on T2 and flare. On MR venography there was a thrombosis seen in the straight sinus. So this was a straight sinus thrombosis. Newborn 45 day old baby presented symptoms of raised ICT refused to feed examination shows sun setting. Clinical diagnosis was meningitis or encephalitis. On T2 weighted sequence mixed intensity lesions seen in the mid frontal region on T2 and T1 also. Coronal T2 also shows very nicely a mixed intensity lesion in the mid frontal region. GRE shows blooming, diffusion source restriction which appears hyper intense on ADC. So this was classical non accidental injury. 45 year old male patient presented with left sided tatexia and tremors of left upper and lower limb with dysmectria. No nystagmus history of CNS tuberculosis 3 years back for which completed course of AKT was taken. Clinical impression was relapse of CNS tuberculosis in posterior fossa, abnormal signal seen in the region of the just anterior to the fourth ventricle. On T2 weighted image these lesions were hyper intense with hyper intense valve. So this was classical hypertropic olivary degeneration. So diagnosis T2 hyper intense lesion confined to olivary nucleus with lack of enhancement or diffusion restriction associated with lesions in contralateral dented nucleus, contralateral superior cerebellar peduncle, axilateral red nucleus, axilateral pontine tegmentum. So we have covered almost all conditions which mimics tumor. Thank you.