Pseudoprogression is a subacute treatment-related effect with MRI features mimicking those of tumor progression. Patients can present with an increase in contrast enhancement and peritumoral edema at MRI. The diagnosis of pseudoprogression is typically made retrospectively on the basis of spontaneous improvement or stabilization of imaging findings without intervention.

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Pseudoprogression typically develops in the setting of combined RT and temozolomide therapy for high-grade or low-grade glioma. but is also observed with immune checkpoint inhibitors in combination with RT for brain metastases and in cases where chemotherapy-infused wafers were placed in the surgical cavity. Pseudoprogression usually develops within 3 months after completion of chemoradiation therapy and is often clinically asymptomatic. The timing of pseudoprogression is earlier than the typical period in which radiation necrosis is described after RT alone; therefore, it is often classified as an early delayed reaction to radiation. Pseudoprogression is most likely induced by a marked local tissue reaction with an inflammatory component, edema, and abnormal vessel permeability causing new or increased enhancement at MRI. Pathologically, pseudoprogression is found to correspond to gliosis and reactive radiation-induced changes without evidence of viable tumor

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The only method of distinguishing pseudoprogression and true tumor progression is to perform follow-up examinations of the patient because conventional MRI does not allow differentiation of the two conditions. Imaging may be regularly performed at 2–3-month intervals throughout the follow-up period although the frequency of imaging can be variable across institutions.

In clinical practice, the following features can be helpful: (a) presence of symptoms and (b) methylation status of the MGMT gene promoter. REF;Nov 20 2020 https://doi.org/10.1148/rg.2021200064

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The current standard treatment protocol for glioblastomas is surgical resection followed by 6 weeks of radiation therapy plus concomitant temozolomide chemotherapy (CCRT) and 6 cycles of adjuvant temozolomide chemotherapy. This protocol increases median survival from 12 to 15 months.  Tumors with hypermethylation of the O⁶-methylguanine-DNA methyltransferase promoter gene show pseudoprogression more frequently. Enlarged enhancing lesions on conventional MR images may actually represent pseudoprogression in up to 46.8%–64% of cases.

The Response Assessment in Neuro-Oncology (RANO) Working Group proposed that within the first 12 weeks of completion of radiation therapy, when pseudoprogression is most prevalent, tumor progression can only be determined if most of the new enhancement is outside the radiation field or if there is pathologic confirmation of progressive disease.

MR imaging techniques such as DWI and dynamic susceptibility contrast PWI. On DWI, ADC values are higher in necrotic tissue than in recurrent tumor tissue because of the high cellularity of tumor tissue. However, the use of DWI is limited due to the heterogeneity of tumor content. Reduced diffusion represents not only highly cellular tumor areas but also inflammatory processes.

On PWI, high relative cerebral blood volume (rCBV) is considered active neovascularization and viable tumor. rCBV > 1.47 had 81.5% sensitivity and 77.8% specificity for differentiating pseudoprogression from tumor progression. However, rCBV analysis has limitations because most lesions have variable tumor fractions; therefore, mean rCBV and histogram-based metrics may be influenced by the rCBV from both tumoral and nontumoral components. Reference : https://doi.org/10.3174/ajnr.A3876

the appearance of enhancing lesions on MR imaging within the first 6 months after completion of chemoradiation therapy poses a challenge because it can reflect true progression (TP) or treatment-related changes known as pseudoprogression (PsP). PsP occurs in approximately a third of all patients with glioblastoma.  Accurate identification of PsP and TP is critical because patients with TP may require a change in therapeutic strategy while those with PsP may not.  The heterogeneity and variability in response did not allow differentiating TP from PsP simply by visual inspection of the parametric maps. However, a quantitative analysis of DTI parameters and rCBV_max from the enhancing regions of the lesion demonstrated better assessment of treatment response in patients with glioblastomas.

Identification of TP

Early identification of TP could prevent further delays in repeat surgery or enrollment in alternative clinical trials. The LRM analysis indicated that the best model to distinguish TP from PsP or mixed responses was based on FA, CL, and rCBV_max. Higher anisotropy values have been reported in glioblastomas compared with brain metastases and primary cerebral lymphomas. High FA in glioblastomas is probably related to the orientation of overproduced extracellular matrix.

Identification of PsP

Accurate identification of PsP is critical for patient management because unnecessary repeat surgery/biopsy can be avoided in these patients and they can continue on an effective temozolomide regimen with standard imaging follow-up of 3–6 months, thereby reducing patient care costs. Logistic regression analysis showed that the best model to differentiate PsP from TP and mixed response included FA and rCBV_max.

Pseudoprogression is predominantly a subacute treatment-related reaction. Pathologically, it corresponds to gliosis and radiation-induced reactive changes including disruption of the BBB, inflammation, increased permeability, and edema. These changes cause increased enhancement on MR imaging and can mimic TP. combination of FA and rCBV_max can help in identifying PsP from TP or mixed response.

Identification of Mixed Response

On a practical level, posttreatment new enhancing lesions usually contain a mixture of viable neoplasm and treatment-induced changes, and a more accurate assessment of the relative contribution of each entity can guide clinical decision-making. However, most previous studies have attempted to only differentiate between PsP and TP. REF; American Journal of Neuroradiology January 2016, 37 (1) 28-36; DOI: https://doi.org/10.3174/ajnr.A4474

Pfeiffer syndrome is a form of pansynostosis of the cranial sutures with associated limb abnormalities. There are 3 types of Pfeiffer syndrome with type I (classic) being the mildest form of the disorder. Midface hypoplasia and abnormal skull shape are minimal in this form of the disease, and intelligence is more likely to be normal in these patients. Type II is more severe and results in the formation of a “cloverleaf” skull (our case), also known as kleeblattschädel, and the degree of cranial abnormality is more pronounced. Pfeiffer syndrome type II is commonly fatal in infancy due to its marked compression on the intracranial structures. Pfeiffer syndrome type III is also more severe than Pfeiffer syndrome type I; however, the cloverleaf skull phenotype is less common in Pfeiffer syndrome type III.

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Pfeiffer syndrome type II is caused by a mutation in the gene for fibroblast growth factor receptor 2 (FGFR2) on the long arm of chromosome 10, a gene that encodes a cell membrane protein responsible for cell differentiation. Pfeiffer syndrome type I has an association with FGFR1, a different gene on the short arm of chromosome 8. Mutations in the FGFR genes are also implicated in Apert, Beare-Stevenson, Crouzon, Jackson-Weiss, and Muenke syndromes, all diseases that exhibit craniosynostosis and/or facial malformations to varying degrees. The pattern of inheritance for Pfeiffer syndrome is autosomal dominant with cases of Pfeiffer syndrome types II and III due primarily to sporadic de novo mutations.

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The cloverleaf skull deformity (kleeblattschädel) was first described by Holtermuller and Wiedemann. The upper and lower leaves of the cloverleaf are formed by a ring of bone that divides the upper and lower leaves of the cloverleaf, and there is a honeycomb pattern of the inner vault of the skull. Crowding of the posterior fossa and subsequent hindbrain herniation are common. Kleeblattschädel can be seen in severe forms of Crouzon and Apert syndromes, Saethre-Chotzen syndrome, Carpenter syndrome, and thanatophoric dysplasia, though Pfeiffer syndrome has been reported to account for approximately 15%-20% of cases. Intellectual impairment observed in patients with cloverleaf skull is most likely a result of the intracranial mass effect from the calvarial deformity rather than an intrinsic brain abnormality, as normal intelligence by 4 years of age has been reported in some cases of patients undergoing a staged reconstruction of kleeblattschädel

The pineal localization is a very rare form of this intracranial lesion. It represents 0,2-1% of all intracranial tumors.  Cushing was the first to report the pineal localization of the epidermoid cyst in 1928. The clinical presentation is often characterized by parinaud’s syndrome and hydrocephalus. Hemiparesis and cerebellar signs can also be noticed

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Otogenic brain abscess may occur as a complication of acute and chronic suppurative otitis media. Radiologists and Otolaryngologists should have a high index of suspicion for otogenic abscesses in patients with a history of chronic ear disease and new symptoms of fever, headache, and nausea.

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Otitis media (OM) is a common otologic condition in pediatric and adult populations. Acute mastoiditis (AM) is a complication of otitis media in which infection in the middle ear cleft involves the mucoperiosteum and bony septa of the mastoid air cells. It can be divided into coalescent and non coalescent mastoiditis. In coalescent AM, infection causes osteolysis of the bony septa or cortical bone, which can further lead to intra and extracranial complications

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The imaging technique of choice is CT for its sensitivity in detecting opacification and bone destruction. Its capability to differentiate among causes of opacification is poor. MR imaging provides additional imaging markers reflecting soft-tissue reaction to infection, major intramastoid signal changes, diffusion restriction or intramastoid, periosteal, or dural enhancement as well as brain abscess.

Complications of OM are classified as extracranial or intracranial. Brain abscess are commonly considered the second most common intracranial complication of OM after meningitis. Historically, it has been reported that 25% of brain abscesses in children were otogenic, whereas in adults it is thought that more than 50% of brain abscesses were otogenic.

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Filum terminale lipomas are increasingly being identified on imaging. The prevalence of isolated LFT is < 5%. There was no significant correlation between the thickness or length of LFT and the presence of neurological deficit. Most patients are asymptomatic and do not require frequent follow-up or surgical intervention