 Good morning, myself, Dr. Dhruv Indoshi, second-year resident at GCS Medical College and guided by Dr. Nikunj Desai, professor at the GCS Medical College. So my topic is MR imaging spectrum of intracranial infections in HIV positive patients. So my aims and objective is to study the imaging spectrum of intracranial infections in HIV positive patients on MRI introduction. HIV is a neurotropic virus that enters the cranial nerve system early in the course of infections. There are three stages in the HIV infection. First is HIV infection primary. Second is latent disease and third it's a disease of the central nervous system in the patient infected with HIV results directly from the virus itself or from the variety of upper genetic agents. Up to 60% of the all patients with AIDS develop the neurological complications. And first manifestation of symptoms, symptomatic HIV infection is in 10 to 20% of the patient when the CD4 counts is false below the 200 cells. So a typical manifestation may be seen due to layering on unmasking phenomenon. So we can see HIV encephalitis. So what we can see is AIDS dementia complex is an HIV associated chronic neurodegenerative syndrome. The imaging findings of the AIDS dementia complex are referred as HIV encephalitis. So in the typical MRI, we can see that it is a cortical atrophy with central predominance and x-vecuode ventricular dilatations, symmetrical patchy or confluent T2 and flare hyperintense disease with periventricular or deep fight matter, frontal or predominant lesion, lesions and no enhancement of the mass effect. On MRI, we can see that is a T2 and a flare images shows the bilateral symmetrical periventricular hyperintense disease with some dilatation of the bilateral frontal hauls of the lateral ventricles. On contrast in T1 and post contrast T1, we can see there is no enhancements noted on T1. So basically with given history and the MR findings, we can see there is a diagnosis of HIV encephalitis. So we are going to the second case. The second case is progressive multifocal depot encephalopathy, PML. PML is a progressive demilandering disorder that results from the JC virus infection of oligodendrocytes. Though so the MR findings that includes multifocal asymmetrical areas of T1 and T2 prolongation in the periventricular and subcortical white matter. Involvement of subcortical u-fibers, posterior fossa environment in the one-third of the cases and a faint peripheral enhancement may be seen in the 10% of cases and there may be seen a mass effect, but it is rare, only 10% in cases. So on the T2 and flare, we can see there is a bilateral diffuse asymmetrical, some hyperintense it is and with subcortical involving the subcortical white matter. On the post-contrast studies, we can see there is a faint peripheral enhancement, faint peripheral enhancement. So with the clinical features, we can see there is a the diagnosis as a progressive multifocal depot encephalopathy. These are T1 image and it is post-contrast T1 image. There is mild peripheral enhancement, but it's not clearly, but we can say with the clinical features that it must be this. So the next disease is toxoplasma. Toxoplasma is caused by an obligate intracellular protozoa toxoplasma gondip. In MRI, we can see that a pre-delication of the basal ganglia, thalamus, cortico medialis junction in frontal and parietal lobes, regions appears typically hypo-indent to iso-intensive T2 weighted images with surrounding vasoviric edema. So ring enhancement is noted in post-contrast studies and enhancing eccentric nodule may be seen, may be noted. It is called a target sign. Preference of a hemorrhage helps to differentiate from the lymphoma. So in T2 and flare hypo, T2 and flare hepatitis intensities is seen in the basal ganglia, thalamus and gray white matter differentiation. We can see it is by the arrow. So in the DWI, we can see high signal intensity rims and low signal intensity enters into the lesion. High signal intensity rim with low signal intensity in the lesion. Post-contrast, we can see there is a mild peripheral eccentric nodule enhancement. So the diagnosis is tuxoblasmosis. The next is cryptococcal infections. It is caused by the cryptococcal neoformants and encapsulated yeast-like fungus. The imaging findings may be consist with the manningoncephalitis, cryptococomas, gelatinous pseudosys or hydrocephalosis. Gelatinous pseudosys are iso-intensive to CSF on MR images and primarily located in the mid-brain basal ganglia. No enhancement is noted in the post-gadolinium images. Cryptococcal is present as a masses of the low single signal intensity. It is on T1W images and a high signal on T2 embedded images. An enhancement of the contrast admission is also seen in the cryptococcal infections. So in the MRI, we can see there is a on T2 and flare. We can see that multiple small lesions are seen in the bilateral basal ganglia, which appears hyperindex on T2 weighted and hypoindex on flare images. Now on the T1 post-contrast, we can see there is a peripheral nodule enhancement. So with given history, we can see there is a maybe extrude the other diagnosis and we can say it is a cryptococcal infections. The next is tuberculosis. Tuberculosis is the most common. CNS tuberculosis aids patient results from the reactivation of the previous infection of the or rarely from the newly acquired infections. The common intracranial infestation of the TB include meningitis, tuberculoma, gandulomas, abscess, cerebral ischemia and infuctions. Fewer basal exudates or greater number of acid-fast basili occur in the brain parenchyma and meningitis in the patient with HIV infections. So on a T2 weighted and post-contrast study, we can see there is a meningeal enhancement on the post-contral images. This is a pure case of, clear case, classic case of ring enhancement lesions, which is seen tuberculoma ring enhancement lesions, which is seen in the post-contrast study. This is axial and this is sagittal sections. So we can clearly say it is tuberculomas. So another differential with the ring enhancement lesions like this is a NCC. But on the basis of the clinical correlation, we can differentiate it on with the spectro. We can differentiate it from the spectro MR spectro. So the summary and conclusion with my topic is HIV related immunological disease is classified into direct complication, indirect complication. The development of the neurological complication depends on the variety of the factors, including therapy with the inter-eteroval drugs and the patients of overall degree of immunosuppressions. The common intracranial infections of HIV positive patient include the HIV encephalitis, progressive, multifocal, leucoencephalopathy, tuberculosis, toxoplasmosis and cryptocallin infections. Knowledge of the imaging finding is assured with the various infection agents that involves the CNS in HIV infected patients is important for guiding the treatment and differentiate from the infection pathology. So my topic is over. Thank you for the listening.