Lopez Rippe Julian,  Velez Florez Maria,  Sompayrac Anne,  Reid Janet

Final Pr. ID: Poster #: EDU-046

Our primary goal is to study individual narratives of career pathways to provide insight into the crucial turning points in one’s journey from becoming to being a physician. Read More

Authors:  Lopez Rippe Julian , Velez Florez Maria , Sompayrac Anne , Reid Janet

Keywords:  professional development, curriculum

Dicamillo Paul,  Wien Michael

Final Pr. ID: Poster #: EDU-051

Understanding and identifying cerebral cortical development and related pathology in children is an important skill for interpreting neuroradiology studies. Cortical developmental disease can be broken down into four topics: microcephaly, abnormal cell types, abnormal migration and abnormal cortical organization. After a brief review of cerebral cortex embryology, this educational exhibit will discuss the main pathologies seen in those four categories with illustrative examples from our institution.

Outline:
I. EMBRYOLOGY
A. Formation of the neural plate
B. Primary neurulation
C. Subdivision of tissues
D. Neuron migration
E. Neuron organization

II. CORTICAL DEVELOPMENTAL DISEASE
A. Microcephaly
1) Microcephaly with simplified gyral pattern
2) Microcephaly with thin corpus callosum
3) Microlissencephaly: microcephalic brain with completely smooth, thick cortex.

B. Abnormal cell types
1) Focal cortical dysplasia
2) Hemimegaencephaly

C. Abnormal migration
1) Cobblestone lissencephaly
2) Classic lissencephaly
3) Incomplete lissencephaly
4) Gray matter heterotopia
5) Periventricular (subependymal) nodular heterotopia
6) Focal subcortical heterotopia

D. Abnormal cortical organization
1) Polymicrogyria
2) Schizencephaly

III. SUMMARY / CONCLUSION Read More

Authors:  Dicamillo Paul , Wien Michael

Keywords:  cerebral cortex, development

Finkle Joshua,  Tullius Thomas,  Javadi Ariyan,  Yang Carina

Final Pr. ID: Poster #: EDU-076

Abnormalities of cortical development include a complex and often bewildering variety of pathologies. With substantial overlap in both imaging appearance and terminology, many radiology trainees and other healthcare providers find these entities can be difficult to learn and efficiently retain. We aim to present a clear and streamlined approach to organizing these disorders within a differential. In the process we use high resolution imaging and original artwork to provide:

- A basic overview of the major steps of cortical development.
- A simplified classification of developmental abnormalities based on the affected stage of development.
- An overview of the underlying pathology, imaging appearance, and clinical relevance of each entity discussed.
- Tips for distinguishing malformations with similar imaging appearances and for understanding the nomenclature used in describing the abnormalities.
- Discussion of new and future imaging techniques for evaluating these lesions, including 3T and 3D DIR techniques.


OUTLINE:

- Cortical development: A basic overview

- Disorders of cell proliferation
— Microcephaly and cortical-related findings
— Hemimegalencephaly
— Focal non-neoplastic processes
— — Focal cortical dysplasia
— — Cortical hamartomas
— Cortical neoplasms
— — Ganglioglioma and gangliocytoma
— — DNET

- Disorders of neuronal migration
— The lissencephalies
— Gray matter heterotopia

- Disorders of cortical organization
— Polymicrogyria
— Schizencephaly Read More

Authors:  Finkle Joshua , Tullius Thomas , Javadi Ariyan , Yang Carina

Keywords:  Cortical Development Abnormalities, lissencephaly, polymicrogyria

Guillen Gutierrez Cinthia,  Rodriguez Garza Claudia,  Elizondo Riojas Guillermo,  Hernández Grimaldo Edgar,  Garza Acosta Andrea

Final Pr. ID: Poster #: EDU-018 (S)

Myelination it's a dynamic process through which a lipoprotein sheath that covers the axons develops. It begins at the 4th month of gestation and reaches its maximum at 24 months and occurs from caudal to rostral, from dorsal to ventral, from central to peripheral

Normal myelination by MRI

Sequences
T1 key sequence to evaluate myelination <1 year. The signal reflects the presence of proteins
T2 key sequence to evaluate myelination 1 and 2 years As the myelin sheaths thicken the surrounding interstitial water moves
FLAIR, DP, DTI complementary sequences

T1WI
RN Brain stem, optical tracts, anterior commissure, ventral thalamus, posterior limb of the internal capsule, rolandic and perirolandic gyrus
2 months deep white matter and anterior limb of internal capsule
4 months Splenium, optical radiations become more evident, cerebellar white matter
6 months Genu, body and splenus of the corpus callosum
8 months U fibers in occipital lobes progressing slowly to frontal and temporal at one year of age.
10-12 months Appearance of myelination with adult pattern in T1WI

T2WI
RN Dorsal brain stem, posterior limb of the internal capsule, ventral thalamus, perirolandic gyrus
2 months Posterior internal capsule arm, semiovale centrum and optical tracts
4 months Optical radiation and subcortical white matter
6 months Splenium
8 months Genu, body and splenic corpus callosum, anterior arm of the internal capsule
12 months cerebellar white matter and occipital subcortical U fibers
18 months Frontal white matter. Some residual hyperintense signals around the trigons of the lateral ventricles
36 months Myelination appearance with adult pattern in T2WI

Myelination Terminal Zones
Normal variant of development
Zones of incomplete myelination
Hyperintense, bilateral and symmetric foci in dorsolateral WM to the atrium of the lateral ventricle

Abnormal Patterns
Delayed myelination Situations in which myelination is slow but present.Usually bilateral and symmetric

Hypermyelination Rare pathology, it can be local or generalized. Sturge Webber, epilepsy and late sequelae of perinatal hypoxia.

Hypomyelinization Permanent deficit of the myelin deposit. Unlike the delay of myelination these do not present myelination over time
It can be seen as normal myelination in T1 but with deficit in T2

White matter diseases
Demyelinating diseases They are acquired and have destruction of normal myelin
Demyelinating diseases Hereditary enzyme deficiency that causes abnormal myelin formation, destruction or turnover Read More

Authors:  Guillen Gutierrez Cinthia , Rodriguez Garza Claudia , Elizondo Riojas Guillermo , Hernández Grimaldo Edgar , Garza Acosta Andrea

Keywords:  Development, white matter

Thomas Anna

Final Pr. ID: Poster #: EDU-077

1. Review frequency, relative severity, and age-related mechanisms of pediatric C-spine injuries.
2. Explore peculiarities of the pediatric cervical spine that predispose to different injury patterns than seen with adults.
3. Examine postnatal pattern of cervical spinal ossification.
4. Inspect the craniocervical junction anatomy, its ligamentous support and classic injury patterns.
5. Discuss available imaging recommendations in the workup of pediatric patients with suspected C-spine trauma.
6. Consider select patient scenarios of classic pediatric c-spine injuries. Read More

Authors:  Thomas Anna

Keywords:  pediatric C-spine trauma, craniocervical junction, C-spine development

Turner Steven,  Lopez-rippe Julian,  Reid Janet

Final Pr. ID: Poster #: SCI-003

Many academic radiology leaders now equally value contributions to education and research in their departments. Whereby research generates publications and grants, the accolades from education may be less completely captured in a curriculum vitae (CV). We present a system that collects, organizes, and showcases a real-time record of the radiologist’s education portfolio to guide faculty development and academic promotion. Read More

Authors:  Turner Steven , Lopez-rippe Julian , Reid Janet

Keywords:  Radiology Education Portfolio, Faculty Development, Academic Promotion