 So today's topic key points are to identify the new imaging findings and come to a differential diagnosis based on the bilateral base signal and thalamacilations, pedometer which are hyper intense on T2 and other imaging modalities. So most important we need to narrow down the differentials and there should be a diagnostic algorithm with a structured report, very important. Most of the time residents are keep seeing them just in front of the workstation. You have to know out of your workstation, see the patient, take the history, check for the other serial markers, any blood resistance which is relevant to your study and then start reporting. Don't directly just start seeing the images and start reporting. So most importantly before I start discussing about the pathologies just want to tell a few words about the function of basic ganglia and thalamacilations. Most of the time when we are studying we hardly forget the function of important structures whichever part you are studying especially please go to the function. The main function of basic ganglia is the body-woman control and the main function of thalamacilations is also called as the inner chamber or the meeting place. So it mainly helps in the relief sensation, a spatial sense, a regulation of consciousness, sleep alertness. In case you are not sleeping and you are not completely restless you will definitely be able to see the images. So the components of a basic ganglia mainly include the corded nucleus, the ketamine and the globus pallidus. Briefly about the basket supply which you need to know because we will be seeing cases where there are thrombosis or there is an infarct you need to know which vessel is the thrombosis. So the brief play of the basic ganglia is mainly supplied by the proximal embankment segment of the MCA and other brands from the infrared of the corded or the ACA. The thalamus has predominantly by the posterior circulation. So these are the results which you can go through. So I will start with the cases. So before cases are mentioned protocol is very important. I request the residents to sit in front of the console when the technician is doing the scanning protocol. The technician will ask you, I am seeing some abnormality in T1 or T2. What are the first investigation or the first sequences you want to meet to do then ask. So if you have a good knowledge about the sequences, definitely you will be guiding the technician what are the other sequences you are supposed to do once you have seen any abnormality like hyperintensity of the basic ganglia or thalamus on a T2 or T1. But I always recommend to do a coronal flare sequence followed by if you are suspecting hyperintensity to do a TWD corresponding TDC mapping as a simplified image and other imaging based on the pathology and the history you can do the 3D talk or 2D talk and post contrast when you are suspecting any malignant lesion. There are like around 20 pathologies which commonly affect the base cell ganglia and the thalamus which is quite difficult to discuss in this short moment of time. So we are discussing on 7 cases which are most common in India and you will have these cases in your practical exam and the exam will expect you to answer correctly without differential for these cases. So there is a case one there is a 4 world female complaints of fever and altered sensorium. So given the images over here or you can see there is bilateral thalamus and the base cell ganglia and the brainstem you have seen a T2 hyperintensity. The GRI further imaging was done there was no hyperintensity and then in corresponding diffusion weighted imaging in the ADC it shows a restricted diffusion. First thing is when you sit in front of the console you are seeing bilateral basal ganglia and the thalamus and the base including the brainstem hyperintensity. Always ask the patient history whether it is an adult male or an adult young female what was the history fever from how many days he had altered sensorium, was there any history of any drug intake, was there any other history of trauma or this matter long. Then we are going to start evaluating. Once you are seeing hyperintensity in the basal ganglia, thalamus and the brainstem you need to have narrowed down your differences and if possible come to a near conclusion diagnosis based on MR imaging. Just don't describe bilateral symmetrical basal ganglia and thalamus and this is noted as a clinical correlation. Even the clinician can make a reserve hyperintensity as a resident try to evaluate the patient take your history value then come to the imaging and then to a near possible diagnosis. So lab in the discussion showed there was a serology positive for Japanese encephalitis. This was a classical case of a Japanese encephalitis. Next case number two you have a 21 year old postpartum complaints of headache, vomiting and seizures. These are the classical case but very important day in and day out. You would be seeing these type of cases especially postpartum lady complaining of headache, vomiting and seizures. So always we do a T2 rated imaging and then your flare and diffusion rate it using bilateral thalamus and the base ganglia hyperintensities including the flare is seeing similar hyperintensity and the diffusion rate is a restricted diffusion and further imaging shows the ADC is showing a low value in the grade cerebral brain. Once you are seeing a low value in the grade cerebral brain those you need to the MR Vinogram. So this case in MR Vinogram showed there is high intensity in the grade cerebral brain on the straight side. So classical case of a venous infarct. So make it a point usually whenever a suspect of venous infarct usually they would send for a CT and you are suspecting an abnormally definitely take the patient to MR. These are the standard segments of a T2 flare and diffusion and when you are seeing in ADC a low signal always do a MR Vinogram to hold out in thrombosis in the cerebral veins. Okay. Complete case number three, 38 old man, the history of partial hanging, nausea and semi-conscious. The moment you see that history there is a history of partial hanging, semi-conscious. Obviously need to think of HII hypoxia. So when you think of hypoxia what are the things they supposed to evaluate in that brain? Like what are sequences? We are setting point of concern. Okay, hypoxia the patient is due to this. So what are the sequences? As I told you always don't forget to do a flare for an image. So in MR we are seeing that a bilateral palomac and the basal ganglia and the flare hyper intensities and diffusion rates showing class restriction and also in some few areas in it. Right below you can see the diffusion restriction. So an ADC map shows a low significant consistent with cytotoxic edema. So they indeed will be seeing plenty of cases like hypoxia even the carbon monoxide poison. So in the classical case of hypoxia or newborn with hypoxia. So these are mandatory sequence which you are supposed to do, take the correct history and then evaluate the images. Don't directly start seeing the images and start reporting. Talk to the patient, evaluate and then do the reporting. Fine. So case number four, 70 and the whole male complains of involuntary movements involving both the upper limbs. So they are given a history on examination. A KFN is in the cornea. Let's increase, see them in even proper. I don't know how many residents will see the cornea or any of any patient. So most of the time they were documented in the case sheet or in a history of the return of the reference of the return. So make it a point to always check the history, what is there. So when they are seeing involuntary movements of both upper and lower limbs for 70-year-old male. So always try to look to increase in proper levels and see them and the urine and then try to look if there are any abnormalities in the cornea. Hardly we go out and talk to the patient but make it a point to talk to the patient and see and take your history rather than being different on the patient's history. So what you are seeing is a high point density. T1 and T2 are seeing a flare hyper intensity in the bilateral basal denture as well as the thalamine. The flare imaging was seeing hyper intensity and it is most commonly involved in the ventral atlaspic, ventriloquial nuclei in the bilateral thalamine. So next you are seeing the famous signs to see. Many of the conditions they say the face of a giant panda or a double panda sign they say. So they are classically seen at the mid-brain level where the mesenchilic substancia and the red nucleus show hyper density. This is the red nucleus show hyper intensity. That was the surrounding white matter. So this is a classical case of Wilson's disease. Please read about Wilson's disease. Very important you will always have this case in any of the examiners collection as a shortcase or longcase. You will have a Wilson's disease. The important is to identify the KFM history on examination accordingly. The other important point is to be that T1 high point density, flare hyper intensity and the T2 hyper intensity. We have seen the basal ganglia, the thalamine. Case 5. For a 26 year old priming for complaints of excess vomiting and complaints of altered behaviour like and difficulty in using both intolerance. So MR imaging was done. Again you can see T2 flare and hyper intensity in the bilateral thalamine and the chordate nuclei. So most commonly in this condition what has happened? The thalamine is involved most commonly in the medial thalamine. It is sparing the ladle. So medial thalamine is involved. So we should have some differences. One or two these are hardly which will not affect only the medial thalamine. So diffusion rate showed the stricter diffusion. This was the case of Vardic esophilopathy. Case number 6 40 year old female complaints of type 2 diabetes this is true of fall andphasia and the lab in this case showed a decreased serum sodium level. So quite very important when there is a decreased sodium level you need to always check aspect of osmotic denulation syndrome. So we hardly check the sodium level sometimes the electrode imbalance complaints of diabetic patient. Most you need to always check the serum sodium. So in MR imaging you are seeing the hypo intensity and the bail there is a ganglia and thalamine in the central ponds. The corresponding image in T2 weighted you are seeing hyper intensity is in the basal ganglia as well as the thalamine and the central ponds. So the further imaging corner T2 flare you are seeing the hyper intensities. So the central ponds it is mainly involving the central ponds and it is varying with the periphery. So this was a classical case of osmotic denulation syndrome. Case number 7 a 10 year old boy presented with Corbett third movements from 3 months so MR imaging was done so you see the MR imaging in the bilateral thalamus predominant thalamus is hypo intense on T1 corresponding on T2 it is hyper intense and flare it is hyper intense but it shows diffuse enlargement you see a thalamic such a diffuse enlargement hyper intense on T2 and hyper intense on flare need to always suspect some malignancy. Because in the previous case of waterways or in fact eutilogy or thrombus or whatever they will not be any diffuse enlargement of the thalamus of the basal ganglia but here you are seeing diffuse enlargement of the thalamus. So there is a mass effect in the form of just causing hydrocephalus. So on the ADC it shows increased signal and there is no diffusion restriction so a spectroscopic show increased cooling peaks and decreased NAND care. So this was a classical case of glioma. So very important glioma in India you see plenty of cases in India you should have a very good knowledge about glioma imaging spectroscopic findings, diffusion what is the further management but how is that patient is being treated and recently the patterns have been changed. So an exam also they do ask about one line of treatment if you need to know whether you treat or not whether it is a medical kind of management or it is a surgical kind of management one line about the treatment aspect include an intervention of all the above conditions which we discussed just now about these commonest conditions which you see which have to be. So I will just come to this there are many conditions I just put few representative images if at all we are suspecting infection which is affecting bilateral basal ganglia and thalamus whether infective eutilogy or history of fever and history of loss of consciousness or altered insorium can engage whatever based on history. So infections always think of Japanese sensibilitis we have come up with vaccines in our Japanese sensibilitis not much commonly seen. So again we have hyper intensities in thalamus in the basal ganglia Cerebral malaria so classical case of Cerebral malaria in hyper intensity on flaring bilateral thalamus so malaria definitely it has been diagnosed by the blood look for the parasite so you need to call it to blood whatever investigations with your imaging findings. Then you have fritzfeld jackup disease so classical case it involved bilateral hyper intensity in the basal ganglia and thalamus so fritzfeld and jackup are two different neurosis from Germany. Someone please read about the snakes this total fritzfeld and jackup. So those are two different neurosis from Germany who discovered and coined this hyper intense in the basal ganglia and thalamus so then come in the toxoplasmosis you have severe proliferation edema also involved sometimes the basal ganglia and the thalamus you always have a history inner compromised patient or a HI patient or with large proliferation edema then further evaluate with respect to the classical case of toxoplasmosis then crypto purposes not routine you see mainly you see a crypto purposes among the inner compromised patient then commonly affects the basal ganglia and the thalamus. Coming to vascular what we did is you want to suspect if the patient is complaining of vomiting loss of vision headache other complications you always think of an arterial the thromosis of the artery supply in the thalamus that is mainly the posterior circulation and if the basal ganglia is a reducible artery you need to evaluate them in MR Angegram. If you are suspecting venous at all do if it is a hypo intensity on a GRE imaging or MR venogram so for this honey filling defect or whatever they always suspect the venous involved so HI you know there is a case of like poison or like carbon monoxide poisoning or a partial hanging with a hypoxia so it will commonly affect the basal ganglia and the thalamus so history plays a very important role in coming to a differential when you are leader of drafting the report and again in the postpartum posterior visible insulopathy syndrome the commonly affects the skeletal occipital parietal lobes including the thalamus Coming to metabolic there is 5 to 6 conditions Wilson's disease I told to the pandas and the giant pandas and mainly the copper leeks disease is mainly mitochondrial disorder very common is in less than 2 years each group so you need to check for the basal ganglia hyper intensity and thalamus hyper intensity fast disease again associated with calcium metabolism increased deposition of calcium please read about calcium metabolism and vitamin D the pre-exam soviet question these days what does it tell about the calcium metabolism so when you read about calcium metabolism please read about hypo-hyper parietalism pseudo hyper parietalism and pseudo pseudo they are very favorite questions what is pseudo pseudo what is hypo and hypo the key pasting so in hypo in fast we are seeing hyper intensity in the basal ganglia because of the calcium deposition in fabulous disease so it is a lysosomal store disease usually you see a D1 hyper intensity along with the hyper intensity in the T2 and in the thalamus and then you have poinx and osmodeemolation syndrome I have already discussed about poinx and osmodeemolation you expect sodium imbalance poinx we have already discussed so next coming to neoplasa I have not gone into much detail I have just shown only one representative case of glioma which commonly affects the parietal thalamus with enlargement of the thalamus you have seen always think of malignancy with the relative hydrocephalitis so with the conclude basal ganglia and covalentation the variety of causes most important very important always ask the history rather than seeing the clinicians history know you talk to the patient and the patient attenders and try to elicit the history from how many days the symptoms is the patient already previously what are the other associated ocular disturbance what are the associated please do ask labrate in this plays a very important role as I told you especially for a well since disease for serum copper like is suspecting osmodeemolation serum sodium everything so plays a very important role in labrate investigations and the knowledge of associated findings but all we need to know like typical of this disease will affect parietal basal ganglia and thalamus which disease will affect only the medial aspect of the thalamus which disease will affect only the lateral aspect of the thalamus so when you have a sound knowledge of the MR imaging findings you can go to labrate investigations and the clinical history and make it very easy when you are done the report so narrow down the differences and use specific diagnosis in certain clinical conditions so I would like to end this with this I would highlight this article I want everyone of you to read a graphics and read about the article named differential diagnosis for parietal obnometase of the basal ganglia and the thalamus