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

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

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