Glioma and glioblastoma multiform (GBM) remain among the most debilitating and life-threatening brain tumors. Despite advances in diagnosing approaches, patient follow-up after treatment (surgery and chemoradiation) is still challenging for differentiation between tumor progression/recurrence, pseudoprogression, and radionecrosis. Radiomics emerges as a promising tool in initial diagnosis, grading, and survival prediction in patients with glioma and can help differentiate these post-treatment scenarios. Preliminary published studies are promising about the role of radiomics in post-treatment glioma/GBM. However, this field faces significant challenges, including a lack of evidence-based solid data, scattering publication, heterogeneity of studies, and small sample sizes. The present review explores radiomics’s capabilities in following patients with glioma/GBM status post-treatment and to differentiate tumor progression, recurrence, pseudoprogression, and radionecrosis.

Psychiatric disorders remain one of the most debilitating conditions; however, most patients are never diagnosed and do not seek treatment. Despite its massive burden on modern society and the health system, many hurdles prevent proper diagnosis and management of these disorders. The diagnosis is primarily based on clinical symptoms, and efforts to find appropriate biomarkers have not been practical. Through the past years, researchers have put a tremendous effort into finding biomarkers in “omics” fields: genomics, transcriptomics, proteomics, metabolomics, and epigenomics. This article reviews the evolving field of radiomics and its role in diagnosing psychiatric disorders as the sixth potential “omics.” The first section of this paper elaborates on the definition of radiomics and its potential to provide a detailed structural study of the brain. Following that, we have provided the latest promising results of this novel approach in a broad range of psychiatric disorders. Radiomics fits well within the concept of psychoradiology. Besides volumetric analysis, radiomics takes advantage of many other features. This technique may open a new field in psychiatry for diagnosing and classifying psychiatric disorders and treatment response prediction in the era of precision and personalized medicine. The initial results are encouraging, but radiomics in psychiatry is still in its infancy. Despite the extensive burden of psychiatric disorders, there are very few published studies in this field, with small patient populations. The lack of prospective multi-centric studies and heterogeneity of studies in design are the significant barriers against the clinical adaptation of radiomics in psychoradiology.

Anaplastic lymphoma kinase (ALK)-positive histiocytosis is an uncommon condition, recently considered a separate condition from other histiocytosis by WHO 5th edition. It can involve intracranial structures. This manuscript describes a case of ALK-positive histiocytosis of the cavernous sinus, focusing on the radiologic and pathologic presentation of the entity. Our case had MRI manifestations mimicking meningioma, metastasis, and Langerhans histiocytosis. On CT imaging, benign osseous remodeling of the cavernous sinus was detected, which can be helpful in differentiating it from more common meningioma.

Patients with Alzheimer's disease who have been given monoclonal antibodies targeting amyloid-β (Aβ) (eg, gantenerumab, donanemab, lecanemab, and aducanumab) for scientific purposes may have a spectrum of imaging findings known as amyloid-related imaging abnormalities (ARIA), shown on brain magnetic resonance imaging (MRI) scans. These neuroimaging abnormalities are caused by antibody-mediated destruction of accumulated Aβ aggregates in cerebral blood vessels and brain parenchyma. ARIA may demonstrate as brain edema or sulcal effusion (ARIA-E) or as hemosiderin deposits caused by brain parenchymal or pial hemorrhage (ARIA-H). The current study explores 2 cases with interval development of FLAIR hyper signal intensity along the bilateral corticospinal tracts in the motor cortex/precentral gyri after treatment by aducanumab. We believe this manifestation is a subtype of ARIA-A that has not been explored earlier. Our first case was a 72-year-old woman with a history of HTN and kidney transplant (polycystic kidney) who presented with mild cognitive impairment with clinical findings consistent with early Alzheimer's disease. After receiving 3 doses of aducunumab and experiencing cognition improvement, she underwent a brain MRI because of dizziness and vertigo. The brain MRI demonstrated new FLAIR hyper signal intensity in subcortical regions of precentral gyri (motor cortex) symmetrically as well as trace subarachnoid hemorrhage at the vertex compatible with ARIA-E and ARIA-H. Our second case was an 85-year-old woman with a history of small lymphocytic leukemia which was treated 20 years earlier. After orthopedic surgery 2 years ago, she developed dementia with anterograde amnesia. Since then, Aricept and Namenda have been started, but there have been no improvements in her subjective condition. The initial Amyloid PET/MR imaging showed diffuse cerebral Amyloid deposition. After tolerating 6 doses of aducanumab a safety MRI revealed new bilateral symmetric FLAIR hyper signal intensity in the subcortical motor cortex. Results of our study suggest that the subcortical corticospinal tract is another hotspot for ARIA findings. Hence, these regions might be an unknown site for both the action and adverse effects of aducanumab on amyloid plaques with secondary inflammation. In addition, radiologists must take this phenomenon into the account, and be cognizant that the FLAIR hyper signal intensities should not be misinterpreted as motor neuron disease (eg, amyotrophic lateral sclerosis).