 Let's move on to viruses causing encephalitis. There are about 55 of them which can affect CNS. The common ones are herpes, jabby, rhabdo, measles, and dengue. And this is what we're going to cover. Herpes by far is most commonly you see in routine practice. It happens because of reactivation of herpes simplex virus, which is common in immunocompetent patients. So, you have a virus in the brain which is normally there and can get reactivated. Typically, you get bilateral asymmetric limbic involvement. So, you get these hyper-intensities in the mesial temporal region, subfrontal cortex, and subcortical white matter, and also it can go along corpus carousel. Typically, most of them show restricted diffusion in the initial stage. Hemorrhage is present in about 20% cases, and then the outcome in these patients is bad. Typical location is frontal, mesial temporal, and insular cortex. Compared to that jabby, which is caused by herbivirus, has central involvement. So, you get involvement of thalamine and basal ganglia. Most of them are symmetric. There is association of cystic circuses with jabby because of pandemicity, and then it is asymmetric. So, the larger affection is on the side of where cystic circus is present. Rabies is now extremely uncommon. It is caused by a rabdovirus. This is my own case, and these two are borrowed cases. Typically, you get involvement of basal ganglia, thalamine, hypothalamus initially, and then eventually, when the patient is about to die, you get involvement of brainstem. Subacute slerozing panencapillitis is another relatively common viral infection in our country. It's caused by measles virus years after primary infection or sometimes after vaccination, but few years after getting vaccination. So, you get symmetric and asymmetric hyperintensities. Typically, starting with frontal parietal lobes and then eventually affecting temporal lobe. Outcome is very, very dismal. It's a progressive disorder. Initially, you get brain swelling, and then you start getting atrophy. You get decreased NA, increased choline, and increased myo-NS at all because of demyelination that happens, and then gliosis. Dengue was very, very common in last decade. Luckily, it is getting lesser. Out of the numbers, involvement of CNS is very, very low. So, you get less than 1% affection in dengue in CNS. But it's a very well-known neurological complication of dengue infection. And there are four ways how dengue can affect brain. The commonest way is because of neurotropism. Again, as I said, seen in less than 1% cases. And it presents like encapillitis, myelitis, or meningitis. The second common is about a week or five days after getting dengue, which is immune mediated. So, you can have presentation like guiabari, edema, or optic or lower canal neuritis. When the patient is bad, and in dengue shock syndrome, you can get the metabolic complications like brain edema, cerebral anoxy, also. Hematological, when the platelets really drop, and there is thrombocytopenia or dehydration causing hemoconcentration, then you get sinus thrombosis or hemorrhages in the brain. And this is one such case. This patient came almost after 15 days of getting dengue from outside ICU into our intensive care, succumbed about 3-4 days after getting admitted at our place. What you see here are multiple pettical hemorrhages, large hemorrhage in corpus callosum, and a lot of brain edema all over the place. These are kind of worst case scenario. Majority of them recover well.