 Hello everyone, my name is Dr. Sai Naitasai from Goa Medical College. Today I am going to present case report on neurotoxoplasmosis in a serophosphate patient. So, toxoplasmophones are an intracellular protozoan parasite which is seen to cause severe infections in an immunocompromised patient such as patients living with HIV and disease. Whereas it is seen to cause cyclical infection in an immunocompromised patient. Currently, these patients have highly put on combination anti-detroviral therapy which is seen to cause decrease in both morbidity and morbidity. Our patient is a 40-year-old female, presented to emergency room with bilateral frontal headache and a solitary episode of CJ. 20 years earlier, she was diagnosed with HIV infection. She was put on highly active anti-detroviral therapy, but she was non-compromised for past 2 years. Soon after the admission, patients developed high-grade fever, but otherwise her other vitals were stable. There were no neurological deficits. Lactar puncture was normal. Citi-pocampus was 126 cents per microliter. In immunological and biological studies, it shows increased CRP, and the patient was positive for toxoplasma IgG antibody. Citi-stam was performed at a casualty level, which shows multiple hypodensity with a hyper-density with ceramic pellets and edema. Hypo-density was also noted in the lab frontal region. Ortheregalvation was performed with MRI. On T1-vetted images, hypointense lesions with hyper-intensity were noted in the lab, caudate nucleus and arytochlorosporosis. T2-vetted images revealed hyper-intensity in bilateral basal cancer with extensive pelletage and edema. A region was noted in the lab frontal region with concentric areas of hyper-intensity and a hypo-intense area with surrounding pelletage and edema. T2-vetted images showed this concentric identity in solar, hyper-intense and hypo-intense in the lab frontal region with associated pelletage and edema. Hypo-intensities were also noted in bilateral basal teglia and the right temporal region. It was also seen to involve left hemipause, left medial lobo-temporal bone left basic frontal region and bilateral cerebral hemisphere. On post-contrast study, this region shows multiple, this region shows a ring enhancement. Coming to discussion, neurotoxic blood moses is a common opportunistic infection which is seen in immunocompromised patients such as HIV leads. Imaging helps in anti-treatment. Toxoplasmosis is caused by toxoplasma bone dye which is intracellular protozoa. It is transmitted to humans primarily by the ingestion of cinch to the undercooked meat or the direct contact with the cat's feces. Most infections are seen when the CD4 counts drop below 200 cells per myroliter. Clinical pictures varies from a big, indolent to high, highly reactive with acute encephalitis in immunocompromised patients. Whereas in immunocompetent patients, these acute encephalitis is exterminated. Imaging features will manifest as multiple regions with a pre-dialection for the basal ganglia, LMI, corticomerular lesion and cerebellum. The average size of these regions range from 2 to 3 centimetres. However, larger regions are also rotate. Citi-canal binding shows multiple ill-defined, hypodense regions predominantly in the basal ganglia, LMI, corticomerular lesion and barely available posterior borsal. It is associated to moderate to macphalizal edema. On CCT, this shows ring or modular enhancement in most of the cases. However, the enhancement depends on the status of the CD4 counts. If the CD4 counts are less than 50 cells per myroliter, the enhancement is minimal or absent. The classification in neurotoxic lismosis is rare. However, in some cases, post-crement, there may be a drop like or peak and junky type of classification. Double-close p-date CCT scans shows central filling in p-late energies. Coming to MRI findings, these regions appear as iso-tohypo-intense or pigmentary energies. Hypo-intense ring may be seen in case of hemorrhage or necrosis on T1 material images. Variable signal intensity is noted on T2 and clear images. There may be areas of concentrated alternating areas of hyper-intensity and hypo- or iso-intensive lens on T2 clear images, which is termed as concentrated target site. It is associated with extensive perillational reticulum edema. On T2 clear images, the regions do not resist. However, there may be some peripheral restriction noted. On post-corner scan, dream-like or regular enhancement is noted. Occasionally, there can be eccentric enhancing nodule in a ring-enhancing region called as eccentric target site. And these enhancing nodules represent the collection of the concentrically thickened vessels. In mass spectroscopy, we will sleep in electric peaks and reduce crawling levels. Cat scan and helium spec shows no update. Coming to differential diagnosis. The most important differential diagnosis for neurotoxical diagnosis is primary CNS lymphoma. And other important differential diagnosis includes cerebral metastasis and other infective focus. So how do we rule out neurotoxical diagnosis versus lymphoma in on-image? So there will be multiple regions in neurotoxical diagnosis. Whereas in CNS lymphoma, it is usually solitary. The location in neurotoxical diagnosis includes basal ganglia, thalamine, cortico-modulation, and rarely the posterior posa. Whereas in CNS lymphoma, it shows sub-tapendermal spread including the peri-ventricular white matter and corpus callotone. Enhancement pattern is ring and nodular in neurotoxical diagnosis whereas strong nitrogenous in CNS lymphoma. Neurotoxical diagnosis results do not restrict, whereas in case of CNS lymphoma, it restricts. The average within the region is more common in neurotoxical diagnosis compared to the CNS lymphoma. The idea is to show high value in neurotoxical diagnosis whereas low value in CNS lymphoma. And one spectroscopy will show cooling peak on CNS lymphoma, which is not seen in neurotoxical diagnosis. But aspects can and they don't expect will be pulled for neurotoxical diagnosis and will be fought for CNS lymphoma. These are my references for my paper presentation. Thank you very much.