 Hello everyone, I am Dr. Naveen Kumar, working as Professor of Radio Diagnosis in Chalman Anandran Institute of Medical Sciences, and I am Chief Radiologist and Director of Mahalakshmi and Moran Diagnostics, Private Limited, located at Karygana, Telangana, India. I am very passionate about teaching, so I have started my own YouTube channel, that is RadVisionSNK, which is exclusive radiology channel, please do subscribe and share. And I have expertise in Neuro radiology for the past 10 years, as I have reported more than 150 MRIs. Please do support my upcoming Neuro radiology series in Indian Radiologist YouTube channel. Thank you all. Good evening all. I will be discussing intra-canalysis, both typical and atypical cases. So, coming to history 32 year mail with history of chronic headache, you can see there is a cystic lesion in the left temporal lobe, which is hyper intense on T1, hyper intense on T2, completely suppressed on flare, there is no restricted diffusion on DWA. So, this is a classical case of arachnoid cyst. So, remember arachnoid cyst, they will not show restricted diffusion on DWA. And remember, galactic classification, this falls under type 2 type of galactic classification. And you also, you have to see the membrane surrounding the arachnoid, whether it is complete membrane or any, there is a breach in the membrane. And there will be no restricted diffusion on DWA in arachnoid cyst, whereas there is restricted diffusion on DWA in the epidermal cyst. So, this is other case 44 year mail with history of headache referred to MRI due to mild asymmetry of ventricular CT. You can see there is a intra-ventricular cystic lesion, which is hyper intense on T1, hyper intense on T2, there is no restricted diffusion on DWA, and no blooming on GRE. So, this is a case of intra-ventricular arachnoid cyst. Close differential can be ependymal cyst. Coming to the other case, 16 year mail with history of headache, diplopia, vomiting and unstable gait. You can see there is hydrocephalus, no restricted diffusion on DWA, hyper intense on T1. But here you can see a thin membrane, which is there, separating the rest of the ventricles from the cystic lesion. And on flare also, you can see the thin membrane clearly depicted, separating the cystic lesion from the rest of the ventricles. So, this is also a case of intra-ventricular arachnoid cyst, causing obstructive hydrocephalus. There is no blooming on GRE, v-patient is in situ. So, remember T2 weighted image and flare images are very crucial in differentiating the membrane of the membrane, which helps in differentiating normal hydrocephalus from intra-ventricular arachnoid cyst associated with hydrocephalus. So, this is an intra-ventricular arachnoid cyst associated with hydrocephalus. Next case, 17 year mail with history of chronic headache came with sudden onset of seizures vomiting following trauma. This is also case of arachnoid cyst. But what is the atypical feature in this arachnoid cyst is, there is no restricted diffusion on DWA. This is the cystic lesion in the left temporal lobe. But here you can see there is an extra-axial CSF signal antestatic collection noted against the left frontal temporal lobe convexities, which is not showing any restricted diffusion on DWA, not showing any blooming on GRE. But this extra-axial CSFs containing cystic collection is seen communicating with that of the cystic lesion in the left temporal lobe. So, here the wall of the arachnoid cyst is not well defined. There is breach in the wall of the arachnoid cyst with expulsion or ores of the contents of the arachnoid cyst into the subdural arachnoid space, subdural space. So, this is a case of arachnoid cyst with rupture with subdural hygroma. So, this is not an M-Pyema because there is no restricted diffusion on DWA, not an infected collection or M-Pyema because there is no restricted diffusion on DWA. And this is not hemorrhage because there is no blooming on GRE. So, this is a case of arachnoid cyst with rupture and concurrent subdural hygroma. Next case, 42 year male with history of headaches, scissors and ataxia. You can see there is a cystic lesion in the right CP angle, which is hyperintense on T1, hyperintense on T2, nearly suppressed on flare with few areas which are not suppressed in the periphery, restricted diffusion on DWA and no significant enhancement in the on-IV contrast. So, this is a case of epidermoid cyst. So, this is a case of CP angle epidermoid cyst and this is a classical black epidermoid and not a typical white epidermoid. So, this is a case of CP angle epidermoid cyst and it is a classical black epidermoid cyst which is hyperintense on T1, hyperintense on T2 and restricted diffusion on DWA. So, what is a typical white epidermoid? We will see in the subsequent case. This is 44 year female with history of chronic headaches, scissors and sudden onset of vomiting. As you can see there is a fat containing density or fat density lesion noted in the right frontal lobe causing midline shift. This is the fat containing lesion and this lesion is hyperintense on T1. You can see heterogeneous hyperintense on T1, no restricted diffusion on DWA, even hyperintense on T2 and not completely suppressed on flare and showing blooming on GRE. So, this is a case of atypical or white epidermoid. So, this is fat containing lesion but there is on T1 these atypical or white epidermoid are hyperintense due to high triglyceride content, high lipid content and even high protein content. So, remember this is a case of white epidermoid. Next, 62 year female with history of chronic headaches and scissors. You can see there is a fat containing lesion with eccentric calcification in the left temporal lobe and even along the left cillian fissure. There is adjacent leiosis. The lesion is predominantly hyperintense on T1, suppressed on flare and showing heterogeneous hyperintense on T2 and showing blooming on GRE or SWA images there is blooming on GRE because fat can show blooming on SWA images and even on GRE. So, this is a case of fat containing lesion with eccentric calcification showing blooming on GRE. So, this is a classical case of intracranial dermoid cyst. So, the previous case there is no calcification and here there is a calcification. So, this calcification or any other tooth like structure or hair or other contents can differentiate dermoid cyst from epidermoid. So, remember this is the chart which helps in differentiation black epidermoid, white epidermoid and dermoid cyst. So, I have seen I have shown you three cases which will this is the case of classical black epidermoid this is the case of classical white epidermoid and this is the case of intracranial dermoid cyst. Next, 44 year male with history of chronic headache and sudden onset of scissors and vomiting. You can see here also there is a fat containing cystic lesion noted in the right temporal lobe with eccentric calcification and even tooth like structure noted within the wall of the lesion and here you can see there is a fat droplet noted in the sulci in the superior sections. So, these are the fat droplets noted in the sulci. So, this is a case of intracranial dermoid cyst with rupture leading to fat disseminating into the CSS spaces. So, this may these cases can present as chemical meningitis and thanks to Dr. Manish Jaishwalsar for contributing this case. So, this is intracranial dermoid cyst with rupture leading to dissemination of the fat into the CSS spaces. So, 35 year female with history of chronic headache and multiple cranial palaces you can see there is a cystic lesion in the cisternal spaces that is pre-ponten and pre-medular resistance which is not completely suppressed on flare and showing restricted diffusion on dW. So, this is a case of cisternal epidermoid cyst. So, sometimes the epidermoid cyst is seen in the cisternal spaces and even this is the cyst sequence where you can see this cystic lesion is causing displacement of the third cranial now bilateral cranial now is more on left side and even encasing the left fifth now this is the right fifth now and this is the left fifth now and also this is closely affecting the bilateral seventh now. So, that is why the patient presented with multiple cranial palaces. So, remember cisternal epidermoid cyst can cause multiple cranial now palaces. So, this is a classical case of cisternal epidermoid cyst. Next case this is also a typical epidermoid cyst case 50 to your mail with history of headache seizures and vomiting you can see there is a lesion cystic lesion which is hyper intense on T1 hyper intense on flare showing restricted diffusion on dWA no blooming on GRE showing patchy heterogeneous enhancement. So, this is a case of intraventricular epidermoid cyst with probable rupture because there is hyper intense contents also noted settling down in the ventricle and even associated vasculitis and infarcts. So, this is a case of intraventricular epidermoid cyst with rupture with secondary vasculitis and infarcts. So, sometimes also remember these epidermoid cyst can occur in the intraventricular location and they can also rupture leading to vasculitis and infarcts. So, this is a case of intraventricular epidermoid cyst with rupture leading to vasculitis and infarcts. Next this is a 12 year mail with history of chronic seizures preterm delivery of rare stones. You can see there are multiple cystic areas of gliosis noted scattered in bilateral paratoxpital lobes, there is mild volume loss, there is paucity of white matter and mild asymmetrical dilatation of atrial and occipital hearts of bilateral lateral ventricles and which is not showing restricted diffusion on dWA. So, this is a classical case of HE that is periventricular leukomalacia or cystic periventricular leukomalacia or HE is equivalent. And sometimes in the chronic stages of developing in HE which are nothing but called eulogyria. Next case, 8 year female history of lethargy caesars, delayed milestones, previous history of preterm delivery and delayed cry. You can see multiple cystic foci or cystic regions scattered in cerebral parenchyma which are hyper intense on T1, hyper intense on T2 there is associated mild carpus collageal agencies also and there are abnormal gravity matter differentiation. So, this is a case of classical multi cystic encephalomalacia. So, this cystic periventricular leukomalacia is one entity of HE and this is multi cystic encephalomalacia where you can see large cysts scattered in the cerebral parenchyma associated with abnormal gravity matter differentiation and they can be associated with other carpus collageal agencies. Next 7 year old baby was referred to MRI in view of finding an inter hemispheric cystic lesion in the brain during routine obstetrics scan. The baby cried immediately after birth. So, here you can see there is a cystic lesion between theеди lateral ventricles which is triangular in shape the TPP is pointing towards the foremen of Mbro, and the B is pointing towards the carpus collageal and this lesion is also causing elevation and posterior displacement of the carpus collageal And inferior displacement are inter circulable veins. So, whenever you see a cystic lesion be displaced between the bilateral lateral ventricles with TPP pointing towards the foremen of Mbro and the base pointing towards the carpus collageal connet with internal cerebral veins inferiorly, definitely think of KVM interpositum cyst, KVM vealum interpositum cyst. So, this is a classical case of KVM vealum interpositum cyst. Next 15 year mail with chronic history of caesars cognitive impairment and developmental delay. You can see there is a defect in the pharx. There is a cystic lesion noted along the pharx in the parafalsine location. There are classical tear drop configuration, suggestive of carpus callous allergences. There is wide widening or diverging frontal horns. And here you can see there are interdigitating are an abnormal gravid matter. So, and carpus callous is not clearly visualized in the sagittal sections. So, this is case of a carpus callous allergences with large inter hemispheric cyst. Next two year female with history of delayed milestones, hemiplegia, caesars and intermittent infantile spasms. You can see there is a CSR signal density lesion in the right temporal lobes. And this CSR signal density lesion is communicating with that of the lateral ventricle. So, this is a classical case of poransophilic cyst. And seven year mail with history of delayed milestones and chronic caesars. You can see there is a CSR density cystic lesion communicating directly with that of the lateral ventricle on right side. And there is a CSR abnormal CSR cleft which is seen partly communicating with that of the left frontal horn of the left lateral ventricle. So, this is a classical case of open rich caesars philly and closed lip caesars philly, both in a single case. So, caesars philly you can see there which is lined by abnormal gray matter, whereas poransophilic cyst which is lined by abnormal white matter. So, that is the differentiating point between the poransophilic cyst and the caesars philly. Next other case, ATR male with chronic history of trauma and caesars. You can see there is gliosis and there is a CSR density cystic lesion noted in the right parietal lobe which is causing erosions, remodelling of the bone and even expansion of the bone. And there are defects in the underlying parietal bone. So, this is a case of growing skull fracture or leptomeningal cyst. So, here you can see this is a depicted as growing skull fracture or the classical leptomeningal cyst. Thanks to Dr. Venkatesh for contributing this case. So, this is a classical case of leptomeningal cyst or also known as growing skull fracture. It is a four-year male with macrosophilae, delayed milestones, attack, sea and spasticity. You can see there is a retrosherbillar CSR-signature cystic lesion. There is no restricted diffusion on DWA, hyper intense on T1, hyper intense on T2. There is and completely suppressed on flare. So, a suggestion of CSR-signature cystic lesion in the retrosherbillar location associated with eplasia of the vermis or eplasia or hyperplasia of the vermis and directly the fourth Venkatesh seen communicating with it as the cystic lesion. So, this is a classical case of dandy walker malformation. Next, 35-year female with history of chronic headache and memory disturbances. You can see there is a cystic lesion which is hyper intense on T1, sitting in the foremen of Monroe, hyper intense on T2, no restricted diffusion on DWA, and flare there is peripheral hyper intense ring and central hyper intensity and not showing significant enhancement because it is already hyper intense on T1. So, this is a classical case of colloid cyst. So, location and the cystic lesion characteristics depict this as a colloid cyst. This is the other case which I am showing CT for a easy understanding. So, 20-year female with history of chronic headache and visual disturbances, you can see hyper dense cystic lesion in the foremen of Monroe. And the HE is approximately 55 to 60 HE, no significant enhancement on IV contrast. So, this is also a classical case of colloid cyst, but this is the CT of colloid cyst. Next, 17-year male with history of chronic headache and intermittent scissors. You can see a cystic lesion which is hyper intense on T2 in the left thalamus, no blooming on GRE, suppressed on flare, not completely suppressed on flare, which is hyper intense on T1. There is no restricted diffusion on DWA. So, this is a case of neuroglial cyst. So, this is a neuroglial cyst in a 17-year male. Next, 26-year female with history of headache, vomiting, salt and sensorium, scissors for 10 days, and even there is history of fever and weight loss since one month. Here you can see there is a cystic lesion which is hyper intense on T2, peripheral hyper intense in RIM, and showing adjacent perilligional vasogenic edema. And there is classical restricted diffusion on DWA noted in the central core of the cystic lesion. And on IV contrast, you can see multiple conglomerate ring enhancing lesions noted in the left temporary lobes with adjacent minimal dual thickening optic enhancement. So, this is a classical case of tuberculoma. So, this restricted diffusion in the central core of the tuberculoma is due to caseous necrosis. And these are conglomerate gram lobes which are commonly seen in tuberculomas than NCC. Next case, 12-year male with history of chronic recurrent scissors, you can see multiple cystic lesions noted scattered in cerebral parenchyma, and fewer showing perilligional vasogenic edema, and fewer not showing vasogenic edemia, and fewer showing peripheral RIM enhancement or ring enhancement. So, this is a classical appearance of starry sky appearance which is seen in NCC. So, there are these are various stages of cystic lesions. Some are non-cystic, some are cystic, some are active, and some are inactive, and few are calcified. So, this is a classical case of starry sky appearance seen in Neurocystic circumstances. Next, 35-year male with history of chronic headache came with certain loss of consciousness, scissors and vomiting. You can see there is a cystic lesion which is sitting in the left parietal, occipital lobe. There is peripheral RIM enhancement noted within the lesion and adjacent perilligional edema and even mass effect over the adjacent ventricle. You can see there are classical detached membranes noted within the cystic lesion. These are the detached membranes noted within the cystic lesion, and the peripheral RIM enhancement noted within the wall of the cystic lesion. So, this is a classical case of hydrated cystin brain which is rare nowadays. Next, 26-year female postpartum with sudden onset of severe headache, vomiting, hypertension and double vision. You can see there is a cystic lesion noted in the pituitary gland, replacing the pituitary gland in the cella. There is fluid fluid levels. This is hyper intense fluid in the top and iso-to-hypo intense fluid in the bottom which is showing blooming on GRE. And here also, you can see the fluid fluid levels. And there is peripheral RIM enhancement on IV contrast. So, this is a classical case of pituitary adenoma with cystic degeneration and hemorrhage. And because of this postpartum and these see hand syndromes can be suspected. So, other close differential can be Rathke's cleft cyst. Where in Rathke's cleft cyst, you can see cystic lesion with a nodule within it. So, whenever you see a cystic lesion in the pituitary with nodule in it, then suspect Rathke's cleft cyst. Next, this is an 80-year male with issue of chronic seizures, headache, vomiting and macrosaphalae. You can see there is a solid cystic lesion noted in the cella with supracellar extension. And the contents of the lesion are predominantly hyper intense on flare, heterogeneous to hyper intense on T2. There is no restricted diffusion on dW. So, whenever you see a child with solid cystic lesion in the cella with supracellar extension and even when you see high signal in the on T1 weighted sequencers or which is nothing but a classical case of adamantine omnitrous type of cranioferringioma, which is common in childs. And this classical T1 hyper intense appearance on T1 is due to high protein content, which is seen in the cystic lesion. So, also also classically described as motor oil appearance or motor oil consistency because of high viscosity. So, whenever you see a child with solid cystic lesion in the cella with supracellar extension and even calcification suspect cranioferringioma, which is adamantine omnitrous type and other type is papillary type, which can be seen in adults. Coming to 2 year mail with issue of macrosaphalae, motor delay, gradual onset of ataxia, spasticity and extracurricular symptoms, you can see there is a diffuse expansion of the white matter, which is predominantly hyper intense. So, this is classical spongiform degeneration of the white matter, which is causing expansion of the white matter, compression of the guyray and even causing the macrosaphalae. And here you can see there are C.S.S. signal intestine cystic lesions noted classically in the antero-middle temporal lobes or sitting in the antero-temperal lobes, which are hyper intense on T2 and completely suppressed on flare and no reshifted diffusion on D.W. in the white matter. So, whenever you see these type of cases where you can see diffuse expansion of the white matter, macrosaphalae and cystic lesions in the antero-temperal lobe or antero-middle temporal lobe, suspect megalencephalic leuconsollopathy with subcortical cysts or van der nap disease. So, this is a classical case of van der nap disease and the close differential can be vanishing white matter disease or Kana van's disease, where Kana van's disease will not find any classical cystic lesions in the antero-temporal lobes or antero-middle temporal lobes. So, this is van der nap disease, which is autosomal recessive disorder and close differentiation is Kana van's disease. 35 female with hitch of hearing loss, tinnitus, vertigo, headache and abnormal care. You can see there is a solid cystic lesion in the CP angle, which is heterogeneous to hyperintense on T2 and showing no enhancement in the cystic component with heterogeneous enhancement in the solid component. So, this is a classical case of CP angle acoustic schwannoma. Next 26 year male with history of chronic headache and intermittent seizures, you can see multiple cystic foci scattered in the left temporal lobe and even reaching up to the sylvan feature, which is causing mild mass effect on the frontal lobe. So, these are classical gaint VR spaces. So, this is a case of gaint VR spaces or tumor effective VR spaces. Sometimes they can even mimic a cystic neoplasm, but no restricted diffusion on WWE, no enhancement on IV contrast can differentiate gaint or tumor effective VR spaces from cystic neoplasms. Seven year male child with chronic history of headache, intermittent warnings, weight loss for six months, the sudden onset of back pain, attacks and urinary retention with weakness. So, here you can see there is a cystic lesion sitting in the floor of the fourth ventricle. There is no restricted diffusion on WWE, which is hyperintense on T2 with peripheral iso to hyperintense rim, no blooming on GRE. And here you can see this is the solid cystic lesion in the fourth ventricle, which is also extended into the CSS space of the upper saropnoid space with significant cord edema. On IV contrast, there is no enhancement in the cystic component, but there is minimal heterogeneous enhancement in the peripheral solid component. Here you can see this is the classical heterogeneous enhancement and the cystic lesion is also seen squeezing the postophosa into the CSS spaces of the upper spinal cord or saropnoid space. So, this is a classical case of ependymoma. So, ependymoma remember there is solid cystic lesion arising from the floor of the fourth ventricle, no restricted diffusion on WWE, and propensity to enter into the CSS spaces and plastic type of tumor, which is trying to squeezing out of the fourth ventricle into the CSS spaces is very pathognomonic of ependymoma. And here you can also see an enhancing nodule in the saropnoid space in the spinal cord. So, this is a case of ependymoma with drop metastasis. Here this is the drop metastasis. Ten year male child who came with history of chronic headache, vomiting, sweat loss since six months. You can see there is a solid cystic lesion in the postophosa and the cerebellum. This is the on IV contrast, you can see there is a solid enhancing or mural nodule. So, whenever you see a solid cystic lesion with enhancing mural nodule in the postophosa, suspect palesitic astrocytoma. And this is causing compression of the fourth ventricle with resultant dilatation of the supra-tentorial ventricular system. So, this is a classical case of palesitic astrocytoma. 26 year female came with chronic history of headache, vomiting, misdiagnosis, weakness in upper and lower limbs, intermittent abdominal pain since eight months. So, here you can see there is a cystic lesion with enhancing peripheral nodule or mural nodule in the cerebellum. And here you can see there is a enhancing nodule-like structure also noted in the spinal cord. So, this is a classical case of hemangioblastoma with drop metastasis. But what is the importance in this case? There are multiple cystic focades scattered in the pancreas and even in the kidneys. So, this is a case of one hippolinda disease with cerebellar hemangioblastoma and even drop metastasis. So, I want to show one mnemonic which has been framed by me to remember all the causes of drop metastasis. Already in the previous case, we have seen ependymoma. So, remember champagne. So, where C stands for corioplexus carcinoma, H for hemangioblastoma as we have seen in this case, A for anaplastic astrocytoma, M for medulloblastoma, P for pineositoma, P for pineoblastoma, P net, G for GVM or germinoma, E for ependymoma. Next, 6 to 10 year male with chronic history of smoking, cough, loss of weight, appetite, came with certain onset of unconscious and seizures. You can see there are multiple cystic focades scattered in volatile cerebellar parenchyma showing peripheral remanagement and showing significant choline peak with even lactate peak or inversion of lactate in the necrotic areas and choline peaks in the peripheral rim areas. So, considering the history of chronic smoking, elderly age with multiple cystic focades with raised choline, these are nothing but classical of cystic metastasis and primary could be in lung carcinoma because of the history. So, I think I have covered various cystic lesions in the brain both including typical and atypical presentations and I thank Dr. Sanjeev Manisar for giving me this opportunity to present in Indian radiologist. Thank you all.