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The coronavirus disease 2019 (COVID -19) pandemic caused by the novel severe acute respiratory syndrome coronavirus (SARS-CoV-2) has affected almost every country in the world, resulting in severe morbidity, mortality and economic hardship, and altering the landscape of healthcare forever. Although primarily a pulmonary illness, it can affect multiple organ systems throughout the body, sometimes with devastating complications and long-term sequelae. As we move into the second year of this pandemic, a better understanding of the pathophysiology of the virus and the varied imaging findings of COVID-19 in the involved organs is crucial to better manage this complex multi-organ disease and to help improve overall survival. This manuscript provides a comprehensive overview of the pathophysiology of the virus along with a detailed and systematic imaging review of the extra-thoracic manifestation of COVID-19 with the exception of unique cardiothoracic features associated with multisystem inflammatory syndrome in children (MIS-C). In Part I, extra-thoracic manifestations of COVID-19 in the abdomen in adults and features of MIS-C will be reviewed. In Part II, manifestations of COVID-19 in the musculoskeletal, central nervous and vascular systems will be reviewed.

Calvarial abnormalities are usually discovered incidentally on radiologic studies or less commonly manifest with symptoms. This narrative review describes the imaging spectrum of the abnormal calvaria. The extent, multiplicity, and other imaging features of calvarial abnormalities can be combined with the clinical information to establish a final diagnosis or at least narrow the differential considerations. Prior trauma (congenital depression, leptomeningeal cysts, posttraumatic osteolysis), surgical intervention (flap osteonecrosis and burr holes), infection, and inflammatory processes (sarcoidosis) can result in focal bone loss, which may also be seen with idiopathic disorders without (bilateral parietal thinning and Gorham disease) or with (Parry-Romberg syndrome) atrophy of the overlying soft tissues. Anatomic variants (arachnoid granulations, venous lakes, parietal foramina) and certain congenital lesions (epidermoid and dermoid cysts, atretic encephalocele, sinus pericranii, and aplasia cutis congenita) manifest as solitary lytic lesions. Other congenital entities (lacunar skull and dysplasia) display a diffuse pattern of skull involvement. Several benign and malignant primary bone tumors involve the calvaria and manifest as lytic, sclerotic, mixed lytic and sclerotic, or thinning lesions, whereas multifocal disease is mainly due to hematologic or secondary malignancies. Metabolic disorders such as rickets, hyperparathyroidism, renal osteodystrophy, acromegaly, and Paget disease involve the calvaria in a more diffuse pattern.

Notochord formation begins between the third and fourth weeks of embryonic development. As the axial skeleton develops, the notochord regresses and eventually contributes to the formation of the nucleus pulposus of the intervertebral disks. Notochord regression can be variable, especially at the 2 poles of the skeleton, which results in the persistence of ectopic notochordal remnants. These remnants include benign entities (eg, ecchordosis physaliphora, benign notochordal cell tumor, Tornwaldt cyst, canalis basilaris medianus, fossa navicularis) or malignant lesions (eg, chordoma). We present a review of these lesions, their clinical presentations, and their typical radiographic appearances. Notochord remnants may have overlapping features in terms of their location and appearance; however, differentiation is crucial because the proper treatment and management may differ drastically. Familiarity with notochord development aids in understanding the characteristic locations of notochordal remnants. Noting the unique imaging findings of notochordal remnants can often help narrow the differential diagnoses.Learning Objective: To describe notochord development, normal regression during fetal life, and notochord remnants that give rise to anatomic variants, including benign and malignant lesions.

Purpose: To report one case of homonymous paracentral scotoma with corresponding optical coherence tomography (OCT) findings in a young woman after injury to the left occipital lobe tip. Observations: A young woman with past medical history of Hodgkin's lymphoma and large B-cell lymphoma metastatic to the left occipital lobe status post resection presented to the eye clinic with a chief complaint of a “blind spot” in the right eye since her surgery. Humphrey visual field (HVF) showed a right homonymous paracentral scotoma corresponding to the non-decussating and decussating optic radiation for central vision originating from the left lateral geniculate nucleus (LGN). OCT confirmed atrophy of the right nasal hemifovea with fibers originating from the papillomacular bundle and the left temporal hemifovea with fibers originating from the superior temporal segment of the optic nerve. These fibers correspond to the central vision involved with the left posterior occipital lobe tip. Conclusions and Importance: We report a case of right homonymous central vision loss as a result of injury to the left posterior occipital lobe tip with certain unique features. Here, a small lesion in the posterior visual pathway led to a relatively large loss of ganglion cell layer. Keywords: Ganglion cell layer, Nerve fiber layer, Homonymous hemianopia, Thinning

The coronavirus disease 2019 (COVID-19) pandemic caused by the novel severe acute respiratory syndrome coronavirus (SARS-CoV-2) has affected almost every country in the world resulting in severe morbidity, mortality and economic hardship, altering the landscape of healthcare forever. Its devastating and most frequent thoracic and cardiac manifestations have been well reported since the start of the pandemic. Its extra-thoracic manifestations are myriad and understanding them is critical in diagnosis and disease management. The role of radiology is growing in the second wave and second year of the pandemic as the multiorgan manifestations of COVID-19 continue to unfold. Musculoskeletal, neurologic and vascular disease processes account for a significant number of COVID-19 complications and understanding their frequency, clinical sequelae and imaging manifestations is vital in guiding management and improving overall survival. The authors aim to provide a comprehensive overview of the pathophysiology of the virus along with a detailed and systematic imaging review of the extra-thoracic manifestation of COVID-19. In Part I, abdominal manifestations of COVID-19 in adults and multisystem inflammatory syndrome in children will be reviewed. In Part II, manifestations of COVID-19 in the musculoskeletal, central nervous and vascular systems will be reviewed.

Background and purpose Carotid artery webs are shelf-like protrusions of intimal fibrous tissue arising from the posterior wall of the carotid bulb, found to have a 2.3% prevalence in the United States (Sajedi et al., 2019). Previous studies have demonstrated its association with ipsilateral anterior circulation stroke. (Labeyrie et al., 2020; Yu et al., 2020) The aim of this study is to assess the prevalence of carotid webs in the largest US epidemiologic study to date, and to further characterize the clinical features of carotid web patients. Materials and methods We assembled a cohort of 1467 adult patients with CTA neck from 1/1/2011 - 1/1/2017. CTAs were reviewed for diagnosis of carotid web. Demographic and clinical details of web patients were obtained. Differences in demographics and CTA indication between patients with and without carotid web were assessed using appropriate statistical tests. Results 24 (24/1467=1.6%) carotid web patients were identified (mean age: 63 years; 62.5% female; 50% African American). Twelve (12/24=50%) had ipsilateral anterior circulation stroke. Of them, 8 were deemed cryptogenic. Four (4/24=16.7%) web patients had at least one recurrent stroke in the ipsilateral anterior circulation. One case was reported on the radiology report at the time the study was initially performed. Conclusion This study confirms a prevalence of 1.6% in our urban, North American cohort. Among carotid web patients, there was a high incidence of ipsilateral anterior circulation stroke, the majority of which were classified as cryptogenic. This study affirms the importance of the diagnosis of carotid web, especially in cryptogenic stroke patients, as a potential unrecognized stroke risk factor.

Background Left‐hemispheric strokes are more frequent and often have a worse outcome than their right‐hemispheric counterparts. This study aimed to evaluate whether cardioembolic stroke laterality is affected by anatomical characteristics of the aortic arch. We hypothesized that laterality varies between patients with bovine versus standard arch. Methods and Results We retrospectively identified 1598 acute cardioembolic strokes in patients with atrial fibrillation from our institutional stroke database (2009–2017). Inclusion criteria were acute anterior circulation ischemic infarct and availability of both arch and brain imaging (magnetic resonance imaging or computed tomography). Alternative causes of stroke and anomalous arch were excluded. Imaging was reviewed for stroke characterization and laterality and arch branching pattern. Bovine arch denotes a common origin of the brachiocephalic trunk and left common carotid artery. Strokes were classified as bilateral (left or right). Univariate analysis was performed using chi‐square tests. The final cohort comprised 615 patients, mean age 77 years ( SD 11.8 years) with 376 women (61%) and 33% white, 30% black, and the remainder mixed/Hispanic. Standard arch (n=424) stroke distribution was left 43.6% (185), right 45.1% (191), and bilateral 11.3% (48). Bovine arch (n=191) stroke distribution was left 51.3% (98), right 35.6% (68), and bilateral 13.1% (25). Bovine arches were associated with more left‐sided strokes compared with standard arches ( P =0.018). There was an association between black race and bovine arch ( P =0.0001). Conclusions Bovine aortic arch configuration is associated with left hemispheric laterality of cardioembolic stroke. This study enriches the understanding that arch anatomy influences stroke laterality and highlights the need for further research into the causative hemodynamic factors.

Artificial intelligence is a rapidly evolving computerized technology affecting multiple aspects of our lives. It is predicted that artificial intelligence will lead to a fundamental change in practice of many professional fields, including medicine. One of the most significant advances in artificial intelligence involves digital imaging and image recognition. Consequently, radiologists, who work in the most digitalized field of medicine, need to be familiar with this rapidly progressing technology. “Artificial intelligence,” “machine learning,” and “deep learning” are terms that tend to be used interchangeably in terms of advanced computer algorithms, but each has a different meaning. Objectives for this article are to demystify these terms for radiologists and to establish a basic understanding of this topic for the reader. We also discuss the impact that artificial intelligence might have on the field of radiology in the foreseeable future. Although artificial intelligence is unlikely to replace radiologists any time soon (if ever), we explore how this technology could be beneficial to radiologists.

Introduction: North American-ATLL (NA-ATLL) is a distinct genomic and clinical entity when compared with Japanese ATLL. Despite the frequent CNS involvement by this entity there are no prognostication tools to identify variables associated with higher risk. We studied one of the largest NA-ATLL cohorts in the United States at a minority rich ethnically diverse New York City based tertiary care center to identify discrete variables that may be associated with CNS involvement. Additionally, we examined the predictive power of the previously validated International Prognostic Index (IPI) developed for Diffuse Large B-cell Lymphoma (DLBCL) in terms of CNS involvement as well as overall survival in our cohort. In our previous work, we assigned CNS involvement of ATLL if: 1) cerebrospinal fluid (CSF) cytology or flow cytometry was positive; 2) CNS imaging was positive for disease involvement or 3) physical exam was compatible with neurologic involvement. Methods and results: Of 65 NA-ATLL patients (pts), 20 (30.77%) had CNS involvement by ATLL meeting above mentioned criteria. The median age of all pts in our dataset was 59 years. Pts were divided into non- CNS involved NA-ATLL (non-CNS NA-ATLL) and CNS involved NA-ATLL (CNS NA-ATLL) groups. Parameters to predict CNS involvement were outlined as leukocytosis (>11000 per microliter [μL]), elevated acute lymphocytic count (>4000/ μL), elevated lactate dehydrogenase (LDH) (>190 units/liter [u/l]), generalized lymphadenopathy (LAD) defined as involvement of 2 or more non-contiguous nodal sites, elevated corrected serum calcium levels (>10.5 mg/deciliter), bone marrow (bm) involvement and serosal involvement defined as pleural or peritoneal involvement. These variables were chosen given our prior work identifying them as critical to predict OS in our general NA-ATLL population. We then performed the Fisher test of proportions to determine if the variables above mentioned were different between the CNS NA-ATLL and the non-CNS NA-ATLL. We did not find significant associations when analyzing gender (p=0.0535), leukocytosis (p= 0.4001), lymphocytosis (p =0.57), hypercalcemia (p= 0.7661), elevated LDH (p= 0.4898), generalized LAD (p=0.271), serosal involvement (p= 0.05088) or bone marrow involvement (p=1). We only found a strong association when examining ATLL subtypes, being the acute/lymphomatous variant strongly associated with CNS involvement (p=2.226e10 -5). To identify variables that can have an impact in OS in CNS NA-ATLL vs non-CNS NA-ATLL we calculated Kaplan Meier survival curves. We did not find any difference based on age (p=0.23), gender (p=0.95), leukocytosis (p= 0.074), lymphocytosis (p =0.21), hypercalcemia (p= 0.094), elevated LDH (p= 0.37), generalized LAD (p=0.28), and serosal involvement (p= 0.1) in the overall survival. The only significant association we found was bone marrow involvement in predicting poor OS in CNS NA-ATLL group (p= 0.038). Next, we determined IPI scores (age>60, ECOG performance status>2, Ann Arbor stage III/IV, serum LDH score >190 u/L and more than 1 extra-nodal site) in our CNS NA ATLL and non-CNS NA ATLL cohorts. We sought to determine if: 1) this prognostication tool is predictive in NA-ATLL and 2) if these variables can be used to identify CNS involvement in our cohort. CNS pts with a higher IPI score (>3) showed tendency towards a lower survival rate (p=0.089) than non-CNS pts (p=0.3). IPI score of 3 or more was not predictive of CNS involvement in our sample (p=1). Conclusions: NA-ATLL is a rare and protean disease with poor prognosis and CNS involvement is prevalent. With the variables used we did not find clear predictors of CNS associated disease other than patients presented with the lymphomatous and acute subtypes. We also observed than bone marrow involvement portends a dismal prognosis for individuals with CNS involvement. Future studies with a larger cohort could provider further insight on discovering predictors for CNS involvement in NA ATLL. Figure 1 Figure 1. Disclosures Shah: Celgene/BMS: Research Funding; Janssen: Research Funding. Gritsman: iOnctura: Research Funding. Shastri: GLC: Consultancy; Kymera Therapeutics: Research Funding; Guidepoint: Consultancy; Onclive: Honoraria. Verma: BMS: Research Funding; GSK: Research Funding; Incyte: Research Funding; Medpacto: Research Funding; Curis: Research Funding; Eli Lilly: Research Funding; Stelexis: Consultancy, Current equity holder in publicly-traded company; Novartis: Consultancy; Acceleron: Consultancy; Celgene: Consultancy; Stelexis: Current equity holder in publicly-traded company; Throws Exception: Current equity holder in publicly-traded company. Janakiram: Amgen: Honoraria.

PURPOSE The aim of our study was to determine the incidence and risk factors of dural venous sinus thrombosis and epidural hemorrhage in the setting of a blunt trauma causing a calvarial fracture crossing a dural venous sinus. METHODS A retrospective review of 472 blunt trauma patients with calvarial fracture crossing a dural venous sinus was performed. Two hundred ten patients who underwent computed tomography venography were identified and evaluated for the presence of dural venous sinus thrombosis and/or epidural hemorrhage. Site and displacement of fractures, as well as age, sex, Glasgow Coma Scale (GCS) score, and mechanism of injury, were considered for potential predictive value of thrombosis and/or epidural hemorrhage. RESULTS We found a 23% incidence of dural venous sinus thrombosis in patients with a fracture traversing a dural venous sinus. Significant predictors of thrombosis included temporal fracture (38% incidence) and skull base fracture (31% incidence). Occipital fracture not involving the skull base was associated with a significantly decreased risk of thrombosis, with an incidence of 9%. Decreased GCS score and fall from height greater than 10 feet additionally predicted dural venous sinus thrombosis. Significant predictors of epidural hemorrhage included parietal fractures and displaced fractures, although a large percentage of nondisplaced fractures in other bones demonstrated epidural hemorrhage as well. CONCLUSIONS Dural venous sinus thrombosis in the setting of blunt trauma with a calvarial fracture crossing a dural venous sinus has an incidence of 23%. Increased suspicion for thrombosis is warranted in patients with temporal or skull base fractures, low GCS score, and recent fall from great height.

8063 Background: Information on central nervous system (CNS) involvement with NA-ATLL is limited. In this study, we describe CNS involvement in ATLL patients at a tertiary hospital in New York City. Methods: We considered CNS involvement if one of the following criteria was met 1) cerebrospinal fluid (CSF) cytology or flow cytometry was positive 2) CNS imaging was positive for disease involvement or 3) Physical exam findings were compatible with neurologic involvement. Results: Of 94 NA-ATLL patients, 21 (22.3%) had CNS involvement by ATLL. CSF was involved in 13/21 and 5/21 patients at diagnosis and relapse respectively. At diagnosis, MRI showed CNS involvement in brain and spine in 5/21 (24%) and 3/ 21 (14%) cases respectively. At relapse, imaging revealed brain and spine involvement in 2 patients each. Neurological exam was abnormal in 7 (33%) and 3 (14%) cases at diagnosis and relapse respectively. Next generation exon targeted sequencing was performed in 9 cases. Table shows the mutations (mtn) and functional groups with frequencies. XPO1 E571K mutation was present in 2 patients with extensive CNS disease and refractory to conventional treatment with an overall survival (OS) of 2 months. To our knowledge, this is the first time that XPO1 E571K is reported in a T-Cell malignancy. We also describe here a second set of mutations with CNS involvement (KLF2 and PI3KCD) in 2 patients. Median OS was 8.5 months, Median RFS was 6.5 months in our series. In most cases, the lymphomatous phenotype appeared to have direct mass-like extension (5/21) with several cases of accompanying osteolytic spine or skull lesions, whereas cases with hematogenous involvement tends to spread to the CSF by traversing the brain blood barrier. Conclusions: In this report we describe patterns of CNS involvement in ATLL and the associated mtns. We also describe two unique cases of XPO1E571K mtn in a TCL. [Table: see text]

Intraventricular neurocysticercosis is an uncommon entity which may become symptomatic due to cerebrospinal fluid flow obstruction. Migration of intraventricular cysts through the ventricular spaces is a rare occurrence. This phenomenon is poorly understood but may be due to pressure changes within the ventricular cavities. We present a patient with intraventricular neurocysticercosis with paradoxical transaqueductal migration of the cyst from the cerebral aqueduct to the fourth ventricle shortly after ventricular drain placement for acute hydrocephalus. The patient also presented with a coincidental sellar and suprasellar mass, later pathologically proven to be a pituitary adenoma. The migration of this cyst resulted in spontaneous relief of obstruction at the cerebral aqueduct, thus restoring normal cerebrospinal fluid pathways and avoiding permanent shunting. We discuss the possible mechanisms and implications of cyst migration, and the diagnostic challenges of concomitant findings of a pituitary mass and neurocysticercosis. Although the presence of a sellar and suprasellar mass in a patient with known neurocysticercosis should raise clinical suspicion for the possibility of sellar neurocysticercosis, pituitary macroadenoma is a more common entity and a more likely etiology for a sellar lesion.

Background Mild head injury (MHI) complicated by an intracranial hemorrhage (ICH) is a common cause of hospital admission after head trauma. Most patients are treated nonoperatively, remain neurologically stable, and are discharged uneventfully. However, a small percentage of patients suffer delayed neurological deterioration (DND). Little is known about the characteristics of DND after an MHI complicated by ICH. Objective To identify the cause, temporal course, and outcomes of patients who deteriorated neurologically after presenting with MHI and ICH. Methods A retrospective review was performed of all adult patients presenting over 54 consecutive months with MHI and ICH. Patients who were treated nonoperatively after initial head computed tomography and had a subsequent DND (Glasgow Coma Scale score decrease ≥2) were identified. Demographics, neurological status, clinical course, radiographic findings, and outcome data were collected. Results Over 54 months, 757 patients with MHI plus ICH were admitted for observation; of these, 31 (4.1%) experienced DND. Eighty-seven percent of patients deteriorated within 24 hours after admission. Twenty-one patients (68%) deteriorated as a result of progressive intracranial hemorrhage, and 10 patients (32%) deteriorated as a result of medical causes. Seven patients (23%) died. Variables significantly associated with mortality included age > 60 years, coagulopathy, and change in Marshall computed tomography classification. Conclusion The incidence of delayed neurological deterioration after MHI with ICH is low and usually occurs within 24 hours after admission. It results in significant morbidity and mortality if it is the result of progressive intracranial hemorrhage. Further research is needed to identify risk factors that can allow early detection and improve outcomes in these patients.

Sturge-Weber syndrome is a neurocutaneous syndrome with a facial port-wine nevus and neurologic features, typically including seizures and hemiparesis. Glaucoma may also occur. MRI features include leptomeningeal angiomatosis, cortical and pial calcifications, and angiomatous change of the choroid plexus. We reviewed a subset of patients with Sturge-Weber syndrome with the rare finding of deep venous occlusion, and present such a case, unusual by comparison to previously reported cases of Sturge-Weber syndrome with deep venous occlusion. Six previously reported cases were reviewed. All cases presented with seizures; five of six had evidence of leptomeningeal angiomatosis; half had cerebral hemiatrophy. This report presents a unique case lacking clinical seizures, but with a port-wine stain and congenital glaucoma. This patient lacked the radiologic findings of leptomeningeal angiomatosis and hemicerebral atrophy, but demonstrated deep venous occlusion with frontal venous collaterals. There is a wide spectrum of findings in Sturge-Weber syndrome. The lack of seizures and angiomatosis in this case are likely "true-true" and related. The case illustrates the unusual finding of deep venous occlusion in Sturge-Weber syndrome occurring without leptomeningeal angiomatosis. Additionally, it demonstrates that although the initial evaluation is normal, patients may later manifest clinical characteristics of Sturge-Weber syndrome.