 Good afternoon, everyone. I'm Dr. Marisela Carvalho, junior resident, Department of Radial Diagnosis Coher Medical College. Today, I will be presenting a case report of a multifocal primary glioblastoma in a young patient. Introduction Glioblastoma, also known as glioblastoma multiform, is the most common and aggressive primary germa that affects 15% of adults, usually seen in older age groups and they mostly present as solitary legions. Following is a case report of a multifocal glioblastoma in a young patient with a misleading clinical presentation that resembled an infected process rather than neuroplasia. Case report A 28-year-old female patient was referred to the emergency department with multiple episodes of seizures and loss of consciousness since one day. Patient also had history of headache and few episodes of fever over the past 15 days. There were no other constitutional symptoms and patient had no other past medical history. On examination, patient had a low GCS with intermittent decorticate posturing. Patient also had a left-sided facial palsy. Under this examination revealed bilateral disc edema. Blood examinations showed a mildly-waste leukocyte count with moderate anemia. Non-contrast CT scan of the brain revealed few hypotense legions in the right temporal and basic temporal region. There was associated white-matter edema and mass effect on the adjacent structures. On subsequently performed MRI, multiple thick walled, well-defined legions were noted in the right temporal parietal region. These legions showed central hypo-intense signal on T1-weighted images with hyper-intensive. Hyper-intensive signal on T2-weighted images with a hypo-intensive rim and hyper-intense on flare with a hyper-intensive rim. Some of these legions showed peripheral areas of restricted diffusivity on diffusion-weighted images appearing low on ADC. Fokai of blooming was seen on susceptibility-weighted images. On injection of gadolinium contrast, thick irregular peripheral rim enhancement is seen of these legions on T1-weighted images. Extensive vasogenic edema is noted in the right parietal temporal-oxidial region. White-matter edema is also seen to involve the entire spleenium as well as the distal body of the corpus chelosum across the midline. Mass effect was noted on the adjacent lateral ventricle with a midline shift and subphalcyne herniation. Descending trans-tintorial herniation with herniation of the right anchors in parahepocampal gyrus was seen with effacement of the ambient system and mass effect on the midbrain. Cerebral edema and early onset hydrocephalus was noted. Multi-vauxil, a mass spectroscopy of the ring enhancing legions was done. Following image shows a choline peak and reduced NAA in the white matter adjacent to the ring enhancing legion, suggestive of a infiltration. The differential diagnosis of the ring enhancing legions in this case included neoplastic etiology and infective etiology. However, the extensive white-matter edema extending across the corpus chelosum as well as the MR spectroscopy findings favored a diagnosis of GBM. Patient was taken to the emergency OT. On-table findings were suggestive of cerebritis with multiple abscesses. Pus culture sensitivity was sent and biopsy samples were taken. Post-surgery, the patient significantly improved and regained full consciousness. Patient was then started on empirical treatment of AKT and antifungals based on the clinical profile and on-table findings. An initial histopathology report revealed acute and chronic inflammation with granulation tissue and treatment was continued. However, a second report from a higher institute was suggestive of astrocytoma NOS-WHO-GRADE-4 that is Clioblastoma and patient was planned for further management of the scene. Discussion Clioblastomas belong to the group of astrocytomas which are primarily malignant tumors of the brain. According to WHO grading system, these are categorized as WHO grade-4 neoplasms. These can be primarily which arise the NOVO, also called IDH wild type, or they can be secondary which arise from a low-grade astrocytoma also called as IDH mutant astrocytomas. Clinical presentation, tumor presents in adults with a peak age group of 55 to 85 years with no gender predilection. Symptoms in presentation include focal neurological deficits and seizures. Symptoms of this intracranial pressure may also be present. Pathology. Primary inglioblastomas can be located anywhere in the cerebral hemispheres involving the subcortical and periventricular white matter. Secondary inglioblastomas have a predilection for frontal lobes. These legions spread across white matter tracts like corpus callosum and corticospinal tracts. Symmetric involvement of the corpus callosum is known as a butterfly glioma. 20% are multifocal with the legions being connected by white matter edema. However, true synchronous or multi-centric tumors are rare. The tumors appear as a reddish-grade tumor in with a central necrotic core. Microscopy shows necrosis and microvascular proliferation which are the hallmarks of GBM. Tumor cells include pleomorphic, fibrilli, astrocytes, gemistocytes and multi-nucleated giant cells. Necrosis and hemorrhage are usually absent in secondary gliomas. Imaging features. On CT, hyperdense central mass with iso-hyperdense rim with heterogeneous rim enhancement is seen. MRI, T1, shows a poorly-marginated mass with mixed signal intensity. T2 and flare sequences, heterogeneous hyperintensity and extensive estrogenic edema. On post-contrast, irregular rim enhancement with non-enhancing necrotic centers. Blooming is seen on susceptibility weighted images. However, most GBMs do not show restricted diffusivity. On MRS, an elevated choline and reduced NEA is seen. Metabolite ratios exhibit relationship to the tumor grade. A little bit lactic peak resonating at 1.33 parts per million is seen in the necrotic areas. Angiography, prominent capillary face tumor blush and large irregular appearing vessels and pooling of contrasts are the features. Spare of tumor occurs along compact white matter tracts, CSF dissemination, epinymel and subepinymel spread, scaldura metastasis, extra CNS metastasis. Treatment includes tumor debulking followed by post-operative adjuvant radiotherapy and chemotherapy. Timely follow-up imaging plays an important role in management. GBM mimics metastasis, multiple well-defined round-ovoid legions located peripherally at gray-white matter junction. MRS also shows a high choline and reduced and naster alaspa date of the legions. However, no spectroscopic abnormalities are seen in the adjacent brain tissue. Absence have thinner regular rims and show restriction on DWI. MRS shows succinate and cytosolic amino acids. Anaplastic astrocytoma and anaplastic oligotendrogrima are hugely difficult to differentiate, requiring biopsy for diagnosis. Pramic CNS lymphoma, often deep-seated with the predilection for the periventricular white matter and corpus callosum, but are rarely necrotic in the absence of HIV AIDS. Tumifactive demyelination is located in subcortical white matter. Peripheral rim enhancement with the horseshoe pattern, open segment facing the sulcus and cortex is seen. Conclusion. Glyblastoma is diagnosed by clinical and imaging findings and confirmed by histopathology. Being an aggressive tumor, it has a poor prognosis, hence early diagnosis and aggressive treatment is essential for a better outcome. In the above case, the clinical profile and on-table findings were suggestive of an infective etiology. However, the imaging characteristics pointed in the direction of a new plastic etiology. It is important to keep in mind the atypical clinical and imaging presentations of GBM in order to avoid delays in diagnosis and treatment. These are my references. Thank you.