Gokli Ami,  Shekdar Karuna,  Reid Janet

Final Pr. ID: Paper #: 174

Both neuroradiologists and pediatric radiologists require unique skills to confidently manage pediatric neuroradiology cases either in a community setting, or in a specialized pediatric tertiary care hospital. We conducted a needs assessment of pediatric radiologists to define their neuroradiology subspecialty training experience and identify perceived skills and knowledge gaps as well as their attitudes toward a customized pediatric neuroradiology curriculum. Read More

Authors:  Gokli Ami , Shekdar Karuna , Reid Janet

Keywords:  Needs assessment, pediatric neuroradiology, training

Prasher Sparsh,  Wigmore Edward,  Surana Snehal,  Vraka Katerina,  Bonney Denise

Final Pr. ID: Poster #: CR-036

Encephalopathy is a well-recognised complication of intrathecal methotrexate in paediatric acute lymphoblastic leukaemia (ALL), often presenting with seizures, altered consciousness, and motor deficits that typically resolve spontaneously within 24–48 hours. In contrast, methotrexate-induced myelopathy is a far rarer and under-recognised entity, with the potential for lasting neurological sequelae if not diagnosed and treated promptly.
We present an unusual case of methotrexate-induced myelopathy in a child with ALL, featuring an atypical clinical presentation and novel MRI findings that expand the recognised radiological phenotype.

A 4-year-old boy in remission from low-risk B-cell ALL (without CNS involvement) received intrathecal and intravenous methotrexate via an atraumatic lumbar puncture. Within hours, he developed left-sided hemiparesis, progressing to quadriparesis, with predominant weakness on the left and brief truncal involvement. He remained afebrile and haemodynamically stable, and laboratory tests, CSF analysis, and methotrexate clearance were all unremarkable. Brain imaging (CT, MRI, MRA) was normal. However, spinal MRI revealed extensive T2 hyperintensity throughout the cervical, thoracic, and lumbar spinal cord, involving both grey and white matter — a pattern more reminiscent of transverse myelitis than classic methotrexate myelopathy. CSF cytology was negative for malignant cells, and autoimmune and infectious screens, including MOG and AQP4 antibodies, were negative. Treatment with high-dose corticosteroids, folinic acid rescue, and IVIG was initiated within 12 hours of symptom onset. The patient showed marked improvement and was discharged ambulant after six weeks, with only mild residual left-sided weakness.

Classic methotrexate myelopathy typically affects the dorsal columns in a caudal-to-rostral progression. In contrast, this case demonstrated diffuse longitudinal cord involvement with mixed grey and white matter changes. Such imaging findings are not widely reported. Histopathological studies in similar cases support a mechanism of superficial demyelination from CSF-contact toxicity, aligning with this radiological presentation.

This case expands the radiological spectrum of methotrexate-induced myelopathy. Recognition of atypical spinal imaging findings is critical for timely diagnosis and early immunomodulatory treatment, which can significantly improve neurological outcomes. Read More

Authors:  Prasher Sparsh , Wigmore Edward , Surana Snehal , Vraka Katerina , Bonney Denise

Keywords:  ALL, Spinal Cord, Pediatric Neuroradiology

Mirza Eushaa,  Aziz Sumaiya,  Ajilogba Kaseem,  Delf Jonathan,  Dickinson Fiona,  Samanta Rajib,  Patel Ushma,  Swienton David,  Sharaf Ahmed

Final Pr. ID: Poster #: CR-044

Case:

We present the case of a 3 year old male patient who presented to ED with right sided weakness and facial drooling post fall with head injury. On examination, there was residual right sided weakness with poor eye contact and communicative difficulties.

Urgent CT Head revealed a focal, well defined hypo-attenuation in the left basal ganglia (Figure 1).

Subsequent MRI Head and Angiogram demonstrated an anomalous origin of the left middle cerebral artery (MCA) and lenticulostriate arteries on Time of Flight (TOF) angiographic images. The left internal cerebral artery (ICA) gives off the left posterior communicating artery which loops back on it giving off a very small MCA and forming a large, odd looking A1 anterior cerebral artery (ACA) (Figure 2). The left lenticulostriate arteries arise on the horizontal segment of the loop which forms the A1 ACA (Figure 2).

The left perforator territory demonstrates high T2/FLAIR signal with diffusion restriction involving the left putamen and upper aspect of the left caudate nucleus as seen on CT (Figure 3).

The patient was initiated on antiplatelet therapy with aspirin. He subsequently represented two months later with transient left sided weakness. Neurological examination was grossly normal apart from a slow gate.

Repeat MRI demonstrated reduction in the extent of the previous T2 signal abnormality within the left putamen consistent with expected evolution of previous infarct (Figure 4).

Dual antiplatelet therapy with the addition of clopidogrel was initiated. Subsequent clinical follow up found improvement in his verbal ability and eye contact.

Discussion:

There are numerous reported anatomical variants involving the MCA, such as a duplicated, accessory and fenestration, which are related to the embryological development of the MCA (1-3). Recently, twig-like MCA’s have been reported which are likely thought to be a secondary consequence to developmental stenosis of the proximal MCA (4). There are currently no case reports describing the anomalous distal ICA, ACA and MCA findings such as those in our case report. We hypothesise that the patient clinical symptoms are likely due to the anomalous origin and tortuosity of the lenticulostriate arteries resulting in hypoperfusion and ischaemia (5). Clinical improvement was demonstrated after initiating antiplatelet therapy. Moreover, interestingly despite the small calibre MCA there was no evidence of ischaemia within this territory. Read More

Authors:  Mirza Eushaa , Aziz Sumaiya , Ajilogba Kaseem , Delf Jonathan , Dickinson Fiona , Samanta Rajib , Patel Ushma , Swienton David , Sharaf Ahmed

Keywords:  Pediatric Neuroradiology, Pediatric Stroke

Holz Emily,  Fisher Paul

Final Pr. ID: Poster #: CR-050

Neurocysticercosis (NCC) is the result of infection of the nervous system by the larvae of Taenia solium—the pork tapeworm. It is endemic in regions of Latin America, Sub-Saharan Africa, and Asia, however, is also of concern in non-endemic regions as a result of immigration and travel to endemic regions. NCC is a major cause of seizures, however disease presentation varies based on the number, growth, and location of lesions as well as the inflammatory response of the host. In addition to seizures, other common clinical manifestations are headaches, intracranial hypertension, focal deficits, and altered mental status. Case Presentation: A 13-year old female with a history of intermittent headaches presented to the emergency department with severe headache, nausea and vomiting, and altered mental status. Upon evaluation, the patient had a Glasgow Coma Scale score of 8, indicative of a severe level of brain injury. A brain MRI revealed a non-enhancing “cystic” ovoid lesion filling much of the third ventricle. A subsequent CT revealed a scolex (anterior end of the tapeworm) with obstructive hydrocephalus at the level of the third ventricle and cerebral aqueduct. NCC has 3 stages—vesicular, colloidal or granular, and calcified—each with characteristic findings on imaging. In the vesicular stage, imaging shows cysts with central hyperdensity on CT representing the scolex. In the colloidal or granular stage, imaging shows cysts with surrounding enhancement and edema, and in the calcified stage, calcifications are visible. In this case, the patient appeared to be at the end of the vesicular stage, transitioning into the colloidal or granular stage as there was evidence of a scolex on CT and a cystic lesion with interstitial edema, however it was non-enhancing. Additionally, in NCC parenchymal lesions are most common, and with antiparasitic treatment, have a generally benign prognosis. Extraparenchymal disease, which includes ventricular cysts as seen in this patient, is less common and is not benign, often resulting in obstructive hydrocephalus, also evident in this patient, and may even result in death. Based on imaging findings, the patient underwent fenestration of the cyst and biopsy, which revealed fragments of a parasitic organism. NCC can result in life-threatening consequences including hydrocephalus, herniation, and edema, so while treatment generally consists of anti-inflammatory and antiparasitic medications, surgery may be indicated in some patients. Read More

Authors:  Holz Emily , Fisher Paul

Keywords:  Pediatric Neuroradiology, Hydrocephalus, Brain MRI

Lee Justine,  Patel Roshni,  Bell Lena,  O'neill Kimberly,  Cohen Benjamin

Final Pr. ID: Poster #: EDU-068

Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) is a condition in which serum antibodies are targeted against central nervous system (CNS) myelin-forming oligodendrocytes, resulting in an acquired monophasic or relapsing-remitting CNS demyelination. The histopathology and imaging manifestations of MOGAD differ from that of other demyelinating disorders, such as Multiple Sclerosis or Neuromyelitis Optica Spectrum Disorders. Age dependent MOGAD presentations have also been reported, in which pediatric patients often present with acute disseminated encephalitis (ADEM) or brain lesions, followed by optic neuritis, among others. This contrasts with that of the typical adult presentation of optic neuritis, followed by transverse myelitis and a smaller proportion presenting with ADEM. Our educational exhibit will showcase the CT and MR imaging spectrum of pediatric MOGAD in patients at our institution, including: 1) ADEM, 2) transverse myelitis, 3) optic neuritis, and 4) other atypical manifestations, including ophthalmologic findings of papilledema.

We also discuss the concurrent finding of elevated intracranial pressure (ICP) in our cases, its presumed pathophysiology in the setting of MOGAD, and brief discussion of the current literature in which little is known about how elevated ICP affects MOGAD disease presentation, prognosis, and management. Interestingly, despite markedly elevated lumbar puncture opening pressures in our pediatric MOG patients, our patients did not demonstrate classic imaging findings of intracranial hypertension, such as those seen in idiopathic intracranial hypertension. This finding is both clinically and radiologically significant, as clinicians aim to better understand the purported disease course, manage MOG-associated intracranial hypertension, and stratify risk in patients demonstrating elevated lumbar puncture opening pressures on admission. Our exhibit will add a neuroradiology imaging component to the literature as we strive to comprehensively understand pediatric MOGAD in the subset of patients who demonstrate associated elevated intracranial pressures. Read More

Authors:  Lee Justine , Patel Roshni , Bell Lena , O'neill Kimberly , Cohen Benjamin

Keywords:  Demyelination, Neuroradiology, Pediatric Neuroradiology

Lara Nunez Denny,  Harder Sheri,  Tshuma Makabongwe,  Azma Roxana

Final Pr. ID: Poster #: CR-056

Fulminant demyelinating diseases include acute disseminated encephalomyelitis (ADEM), myelin oligodendrocyte glycoprotein antibody associated disease (MOGAD), multiple sclerosis (MS) and neuromyelitis optica-spectrum disorders (NMOSD), among others.
The purpose of this case report is to present the evolving MRI/MRS findings in a patient with fulminant MS.

A seven year old female presented with a 3 day history of progressive encephalopathy, gait disturbance and urinary incontinence. She had a recent viral upper respiratory tract infection. Interestingly, family history revealed the diagnosis of multiple sclerosis in the patient’s mother. Brain MRI revealed extensive T2/FLAIR hyperintense lesions, predominantly related to the cerebral and cerebellar white matter, with associated incomplete rim and central enhancement and marginal diffusion restriction. MRS showed decreased NAA, elevated choline and a prominent lactate peak. Accompanying bilateral anterior optic neuritis and papillitis was noted with T2 hyperintensity, enhancement and diffusion restriction.
Immune suppressive treatment was initiated. Short interval serial follow up demonstrated progressive confluence of the lesions with increasing edema. While overall enhancement and diffusion restriction decreased, there was a new leading edge of diffusion restriction and enhancement, mainly in the bifrontal region. A persistent inflammatory signature was demonstrated on MRS. Subsequent follow up demonstrated some cerebral volume loss with resolving edema, enhancement and diffusion restriction.
An extensive autoimmune panel was negative, including aquaporin 4 antibodies, NMO and MOG antibodies. Although CSF was sent for oligoclonal bands (OCBs), the sample volume was inadequate for testing on the first lumbar puncture (LP). OCBs were not identified on subsequent LP obtained after initiation of treatment.

Pediatric MS is defined when the onset is before the age of 16 with less than 1% of patients presenting under the age of 10. Marburg variant is a rare, rapidly progressive, fulminant form of multiple sclerosis with high morbidity and mortality rates. Fulminant ADEM typically presents as a monophasic demyelinating disease and is often preceded by a viral or bacterial infection. In this case, the patient fulfilled Mc Donald diagnostic criteria 2024 for MS with initial typical MS lesions in ≥4 central nervous system topographies. Read More

Authors:  Lara Nunez Denny , Harder Sheri , Tshuma Makabongwe , Azma Roxana

Keywords:  Brain MRI, Pediatric Neuroradiology

Molto Garcia Jose Francisco,  Nair Lakshmi,  Kahn Ilana

Final Pr. ID: Poster #: EDU-104

MOGAD varies widely in MRI patterns and has overlapping imaging features with other conditions such as leukodystrophies, infections or other autoimmune diseases. The 2023 MOGAD diagnostic criteria highlights the diagnostic role of MR imaging to diagnose patients that have low positive myelin oligodendrocyte glycoprotein IgG titers or when the titers are not available. This poster aims to review the various MR imaging appearances of Pediatric MOGAD. We will review the most common phenotypes such as ADEM, optic neuritis or longitudinally extensive myelitis but also others not as common, such as brainstem and cerebellar involvement, leukodystrophy-like or cranial and peripheral neuropathy patterns. We will also provide teaching points and some clues for the differential diagnosis, including the discussion of a pathologic slide of a tumefactive case that led to biopsy. Finally, this poster will highlight the importance of ASL to diagnose cortical forms of MOGAD, which may be subtle on conventional sequences but very apparent on perfusion imaging. We certainly believe that this poster may be of great help to familiarize radiologists working in institutions where MOGAD is not commonly encountered. Read More

Authors:  Molto Garcia Jose Francisco , Nair Lakshmi , Kahn Ilana

Keywords:  MR, Autoinflammation, Pediatric Neuroradiology

Tierradentro-garcia Luis,  Martinez-correa Santiago,  Forero-millan Julian,  Martinez Mesha

Final Pr. ID: Poster #: CR-043

Background:

Pediatric acute-onset neuropsychiatric syndrome (PANS) is a rare neuroinflammatory entity that is often associated with infectious and non-infectious triggers. This condition was first associated with recent Streptococcal infections (PANDAS) in the late 1990s. PANS manifests with sudden obsessive-compulsive disorder and/or restricted food intake with additional neuropsychiatric abnormalities. Children with PANS demonstrate generalized increased median diffusivity in the brain, more prominently in the deep gray matter, including the thalami, basal ganglia, and amygdala. Although neuroimaging plays a supportive role in diagnosis, its use is limited by the lack of positive findings in cases with clinically diagnosed PANS.

Purpose:

We aim to showcase brain MRI findings in a child with a clinical diagnosis of PANS at different time points. Our goal is to build on the potential role of neuroimaging in this condition in the acute and subacute phases.

Case description:

We discuss the case of an 11-year-old boy who presented with fever and altered mental status two weeks after having an upper respiratory infection. The patient underwent a contrast-enhanced brain MRI, which showed increased T2W/FLAIR signal and swelling of the caudate nuclei and putamina bilaterally, with no abnormal enhancement or restricted diffusion; notably, there was mild increased diffusion in the basal ganglia, likely reflecting vasogenic edema. Five days later, a repeat brain MRI revealed mild, diffuse high T2W/FLAIR signal, which was overall decreased compared to the prior scan. Additionally, diffusion in the caudate relatively decreased compared to the putamina. Twelve days later, there was a continued decrease in the T2W/FLAIR signal in the putamina, caudate nuclei, and possibly the lateral portion of the globi pallidi.

Discussion points:

-To present common neuroimaging findings in patients with suspicion/diagnosis of PANS/PANDAS over time, including increased T2W/FLAIR signal and mild increased diffusion in the basal ganglia.
-To discuss the current roles/limitations of neuroimaging in the workup based on the existing literature.
-To illustrate the primary differential diagnoses that can mimic PANS/PANDAS neuroimaging findings in children, including autoimmune encephalitis, Sydenham chorea, mitochondrial disorders, and tic disorders.
-To hypothesize the role of glymphatic, CSF, and venous dynamics in neuroinflammation in PANS/PANDAS related to early vasogenic edema. Read More

Authors:  Tierradentro-garcia Luis , Martinez-correa Santiago , Forero-millan Julian , Martinez Mesha

Keywords:  Pediatric Neuroradiology, Basal Ganglia, Diffusion Weighted Imaging

Soker Tom,  Wien Michael

Final Pr. ID: Poster #: EDU-062

Objectives:
To review normal neonatal brain anatomy as seen on ultrasound.
To review the pathophysiology of common brain injuries in premature neonates.
To detail the utility of ultrasound and MRI in evaluation of common neonatal brain injuries.

Table of contents:
US evaluation of the neonatal brain
–Review standard views
–Review normal neonatal brain anatomy
Pathophysiology of Germinal Matrix Hemorrhage (GMH)
Review of ultrasound and MRI findings in GMH
–Initial injuries, and how they evolve over time
–Sample cases and mimics
Pathophysiology of Periventricular Leukomalacia (PVL)
Review ultrasound and MRI findings in PVL
–Initial injuries, and how they evolve over time
–Sample cases
Summary and key facts Read More

Authors:  Soker Tom , Wien Michael

Keywords:  Germinal Matrix Hemorrhage, Brain Ultrasound, Pediatric Neuroradiology