Neuroimaging in Pediatric Epilepsy

EEG Course 2025

Maksim Parfyonov, MD FRCPC

parfyom@ccf.org

Cleveland Clinic Epilepsy Center

August 16, 2026

Discolosures

None

Objectives

Imaging basics and modalities
Review indications for neuroimaging in pediatric epilepsy
Imaging guidelines suggested by ILAE
Overview of common and less common substrates for epilepsy

Neuroimaging basics

What modalities are available?

Structural: CT, MRI
Functional: fMRI, PET, SPECT
Advanced post-processing techniques (e.g. VBM), novel methodology (MRF)

WHAT are we actually measuring with MRI?

MRI Physics Primer

“Relaxation”

T1 vs T2

Signal Detection

More than you ever wanted to know about MRI physics

MR Sequences

Different sequences highlight different
Dominant weighting: T1-weighted (TR short, TE short) vs T2-weighted (TR long, TE long)
FLAIR - Fluid-attenuated inversion recovery
Diffusion-weighted imaging

Image courtesy of Preston, 2016

WHY is imaging important in epilepsy?

Reasons for Neuroimaging

establish etiology
prognosis
identify an acute process, e.g. hydrocephalus, encephalitis
subacute or chronic process that requires intervention e.g. tumor, or has other prognostic implications, e.g. leukodystrophy
focal lesions may be potentially amenable to epilepsy surgery e.g. MCD
understand anatomical relationship to nearby eloquent regions

Lesional vs Non-lesional epilepsy

Epilepsy surgery success is directly related to precise localization of EZ²
Rate of success in lesional TLE 62-80% vs nonlesional 36%³
Meta-analysis of 40 articles and 697 NL and 2860 LE patients: SZ free odds increased with lesional 2.5 overall, 2.7 temporal and 2.9 extratemporal⁴

Finding a lesion may completely change your approach!

WHEN should we image?

Indications for Structural Neuroimaging⁵

Imaging Indicated	Imaging not indicated
Focal history, abnormal exam, focal EEG abnormalities	Childhood absence epilepsy
Developmental regression	Juvenile absence epilepsy
<2 yrs old	Juvenile myoclonic epilepsy
Symptomatic generalized epilepsy syndrome	SeLECTs (Self-limited epilepsy with centrotemporal spikes)
Increased ICP
Status epilepticus
Atypical course of SeLECTs or IGE

What is the yield of imaging?

New onset seizure and status epilepticus 64/177 children (36%)⁶
Community-based study in Conneticut of children with new onset epilepsy. 488/613 (79.6%) had imaging. Etiologically relevant findings in 62/488 (12.7%)⁷
Abnormal exam or focal EEG increases odds of finding abnormality

HOW to perform MRI in patients with epilepsy?

Recommended protocol

🇨🇦

HARNESS-MRI

⁸

HARNESS-MRI

⁸

HARNESS-MRI Advantatges

High‐contrast, 3D sequences with isotropic voxels (ie, identical dimensions across planes)
Can be obtained on 1.5T and 3T scanners
Applicable to adults and children
Provide complete brain coverage
No need for operator‐dependent slice angulations
Images may be reformatted in any plane without loss of resolution
Improved signal‐to‐noise ratio and tissue contrast

Overview of imaging findings in pediatric epilepsy

Overview

Malformations of Cortical Development
Sequelae of perinatal insult
Mesial temporal sclerosis
Rasmussen Encephalitis
Tumors
Neurocutaneous syndromes

Malformations of Cortical Development

The human brain is a clonal mosaic

⁹

Timing is everything…

⁹

Focal Cortical Dysplasia (FCD)

FCD Classification

¹⁰

Classification Update

New terms
- mild malformations of cortical development (mMCD)
- mMCD with oligodendroglial hypertrophy (MOGHE)
- “no definite FCD on histopathology”
“Layers” of classification: histopathology, molecular/genetic, imaging (e.g. “MRI positive Focal Cortical Dysplasia IIb, FCD gene panel negative”)

FCD Histology

¹¹

Staining with neuronal nuclear antibodies (NeuN). B, FCDIa = abundant neuronal microcolumns with often small neurons vertically arrayed like parallel strings of pearls. C, FCDIb of the temporal lobe without any layered neocortical organization. Also note the dramatically thinned cortical diameter. D, FCDIIb of the frontal lobe is characterized by lack of any cortical layering. Instead, large dysmorphic neurons appear randomly placed throughout the cortical ribbon (arrow). Balloon cells are not visible in this NeuN immunohistochemistry. E, FCDIIIa in the temporal neocortex of a patient with hippocampal sclerosis. Note the neuronal cell loss in supragranular layers L2 and L3 (arrow). F, FCDIIIc in a patient with Sturge–Weber syndrome and a vascular malformation (VM), that is, meningeal angiomatosis. The adjacent neocortex is thin and shows abundant microcolumns (as in FCDIa). G, FCDIIId of the parietofrontal region in a patient with perinatal stroke. Note the patchy disruption of cortical layers (arrow). H, FCDIIId of the occipital region in a boy with perinatal hypoxemic injury. Note the loss of layer 4 neurons (arrow). Scale bar = 500 μm, applies to all images

FCD Imaging - General Features

blurring of the gray-white matter interface
signal change on T2-weighted and FLAIR images
- may indicate presence of balloon cells¹²
abnormal thickness or gyration/sulcation patterns

Where is the lesion?

Voxel-Based Morphometry

MRI post-processing method which gives us 3 volumetric statistical maps¹³:
- junction map
- extension map
- thickness map
Enhances ability to visualize subtle lesions
Still requires human to look at the maps (for now…)

Type 1 FCD

mild hyperintensity of WM on T2/FLAIR
loss of GW matter differentiation
often subtle
more common in temporal
may be associated with lobar hypoplasia, atrophy or cortical thickening¹²

Type 1 FCD

¹²

Type 2 FCD

Range of changes from extremely subtle to obvious
more common in frontal lobe >> parietal/temporal
IIa - focal blurring of GW, may have abnormal gyration/sulcation pattern
IIb - similar to IIa, but often has signal abnormality; can have other signs
Up to 80% seizure freedom for FCD IIB¹²

FCD2A

¹⁴

Bottom of Sulcus Dysplasia

direct implication on surgical approach and outcome
complete resection achieves seizure freedom in most
histopathology: FCD2B, or less commonly FCD2A
characteristic rhythmic spiking on SEEG
imaging - may show transmantle sign

Transmantle sign in FCD IIb

Case courtesy of Andrew Lawson, Radiopaedia.org, rID: 26376

Type 3 FCD

¹⁴

MOGHE

Mild malformation of cortical development with oligodendroglial hyperplasia in epilepsy

Can often present in early childhood, spasms or treatment resistant focal epilepsy
Histopath hallmark is proliferation and increased density of oligodendrocytes
Somatic variants in SLC35A2 gene represent possible biomarker, and therapeutic target¹⁶

MOGHE Imaging Features

Age-related differences
- Subtype I (younger children): increased laminar T2/FLAIR signal at the corticomedullary junction
- Subtype II (older children/adults): reduced corticomedullary differentiation due to increased signal in adjacent white matter, with hypomyelination less apparent

MOGHE Imaging Features

Hemimegalencephaly

rare hamartomatous malformation of the brain with extreme asymmetry
classification: isolated, syndromic, and total
syndromic associations: epidermal nevus syndrome, Klippel-Trénaunay-Weber syndrome, Proteus syndrome, Hypomelanosis of Ito, Neurofibromatosis, Tuberous Sclerosis, and others

Hemimegalencephaly - Imaging

increase in the volume of WM, thick cortex with poor gray-white differentiation
May have elements of lissencephaly, pachygyria, polymicrogyria, schizencephaly
corpus callosum is usually asymmetric, but may be hypoplastic or absent

Total Hemimegalencephaly

Case courtesy of Frank Gaillard, Radiopaedia.org, rID: 6619

Other MCD

Polymicrogyria (PMG)

excessive small gyri and shallow sulci
may be associated with other lesions (e.g. callosal agenesis, PVNH)
etiology varies - pathogenic variants (32%), infection (4.5%), vascular (5.5%), unknown (46%)¹⁷
2.3 per 10,000
Frontal 71%, Parietal 37%, Temporal 34%, Occipital 11%

Bilateral PeriSylvian Syndrome

Congenital bilateral perisylvian syndrome first described by Kuzniecky, Andermann and Guerrini¹⁸
- diplegia of facial pharyngeal, masticatory mucles
- mild to severe cogntive impairment
- epilepsy in 87%
Nice illustration here¹⁹

Bilateral Peri-Sylvian PMG

¹⁹

PMG Spectrum

¹⁷

(A–C) Axial T2 of PMG (solid arrows) with peri-sylvian distribution in three individuals with CMV infection. Black arrows for sylvian fissure. White arrows for PMG. (A) Bilateral peri-sylvian distribution, more severe left then right, with bilateral frontal and less parietal extension with effacement of sulci. Left sylvian fissure opened due to more extensive PMG; (B) bilateral peri-sylvian with predominantly posterior extension with more marked extension in the left than the right parietal lobe causing widening of left subarachnoid space; (C) with parietal and occipital distribution, arrows on superior occipital gyri. (D–F) Axial T2 of PMG after probable pre-natal vascular insult. (D) Left frontal dysgyria and PMG with a deeply infolded heterotopic grey matter brain malformation in the anterior left frontal lobe with anomalous subarachnoid spaces and vessels (not present on the image) with focal PMG also in the right frontal lobe (GS performed, unknown aetiology); (E) right temporal PMG with white matter volume loss and dilated temporal horn of the lateral ventricle (NPHP1); (F) bilateral peri-sylvian PMG (black arrows) with parasagittal volume defect (open arrow) and posterior white matter volume loss with PMG in the left inferior parietal lobe (genetic evaluation not performed).

Schizencephaly

cleft which connects the cortical surface with ventricular lumen
edges are often lined by abnormal cortical tissue
open lip vs closed-lip (edges are juxtaposed vs not)²⁰
sporadic, may be linked to an in utero insult resulting in abnormal neuronal migration
rare familial cases have been reported, EMX2 gene²¹
usually present with some degree of developmental delay, seizures common

Open-lips (A, B) and closed-lips ¹⁴

Periventricular nodular heterotopia (PVNH)

ectopic neurons/gray matter in the periventricular areas (subependymal)
disruption of neuroependyma, impairs neurons from attaching to radial glial cells and impairs initiation of migration
severe LOF variants in FLNA gene, X-linked - almost exclusively female
but PVNH are common and many not associated with FLNA
distribution of nodules can be classified as unilateral/bilateral, anterior/posterior/diffuse
range of clinical presentation: incidental, developmental delay, epilepsy

Periventricular nodular heterotopia (PVNH)

²²

Subcortical band heterotopia (double cortex)

band of laminar subcortical ectopic gray matter
may be continuous or semicontinuous
usually bilateral, symmetric and anterior predominant
failure of neuronal migration
some associated with DCX pathogenic variants (in females; males with this develop lissencephaly)²³
wide range of phenotypes (normal intelligence to severe ID), usually treatment-resistant epilepsy

Subcortical band heterotopia (double cortex)

¹⁴

Perinatal Insults

A note about timing…

important to consider timing of MRI relative to gestational age!

²⁴

Myelination Progression

²⁵

Hypoxic-ischemic encephalopathy (HIE)

Umbrella term for perinatal brain injury
Present as encephalopathic newborns, +/- seizures
Patterns of injury due to HIE depened on timing and degree of ischemia

²⁶

HIE Injury Patterns

²⁷

Sequalae of HIE

²⁸

Sequalae of HIE

²⁸

Sequalae of HIE

Perinatal arterial ischemic stroke

Incidence 20 per 100,000 births per year
Commonly present with focal seizures in neonatal period
Similar imaging features to adult stroke, depend on time from event

Epilepsy after perinatal injury

Only 13% of infants with acute symptomatic seizures develop epilepsy (at 24 months)²⁹
1/3 drug resistant
duration of seizure days on EEG is a risk factor

Mesial Temporal Sclerosis (MTS)

MTS Imaging

common cause of TLE
typical story - remote insult e.g. encephalitis, infection or trauma in first 4-5 years of life³⁰
important to diagnose because surgery often successful (near 90%)³¹
Imaging:
- atrophy of hippocampus on T1w images
- abnormal signal intensity on T2w images
- hypometabolism on FDG-PET
Volumetric measurement may be useful, especially when bilateral disease¹⁴

³²

MTS

¹⁴

Adult vs Pediatric MTS

MTS found in only about 1% of children newly diagnosed with epilepsy⁷
Pediatric temporal lobe epilepsy cases, diagnosed as MTS by MRI - often found to have other pathology after surgery³⁴
Controversy whether febrile seizures cause MTS³⁵

Rasmussen Encephalitis

Rare, progressive disorder characterized by treatment resistant epilepsy, often with neurologic decline and hemiparesis
Poorly understood etiology, neuroinflammatory profile on histopathology
MRI shows progressive atrophy of one hemisphere, often worst in opercular region
Increased signal on T2 and FLAIR

🇨🇦

Rasmussen Criteria

Adapted from Bien 2005³⁶

Part A (Need 3/3)
Category	Criteria
Clinical	Focal seizures (+/− EPC) and unilateral cortical deficit(s)
EEG	Unihemispheric slowing +/− ep.form activity and unilateral SZ onset
MRI	Unihemispheric focal cortical atrophy and \(\geq\) 1 of: - GM or WM T2/FLAIR hyperintense signal - Hyperintense signal or atrophy of the ipsilateral caudate head

Part B (Need 2/3)
Category	Criteria
Clinical	EPC or prog’ve unilateral cortical deficit(s)
MRI	Prog’ve unihemispheric focal cortical atrophy
Histopathology	T-cell–dominated encephalitis with activated microglial cells and reactive astrogliosis

Rasmussen Encephalitis Imaging

Tumors & Tumor-like conditions

Neoplasms

CNS Neoplasms in pediatric patients often present with seizures
Any tumor can present with seizures, but certain types are especially tied to epilepsy: “epilepsy-associated developmental tumors”³⁷
ganglioglioma, gangliocytoma, desmoplastic infantile ganglioglioma, dysembryoplastic neuroepithelial tumor (DNET), and pleomorphic xanthoastrocytoma (PXA)
most contain some glial and neuronal component, low proliferation index, only small percentage may undergo malignant transformation
may be associated with FCD (i.e. FCD type 3)

Epilepsy-associated Developmental Tumors

Similar imaging characteristics:
cortically based
hypo- or iso-intense on T1, and hyperintense on T2
Commonly have contrast enhancement

Dysembryoplastic neuroepithelial tumor (DNET)

much less common than ganglioglioma in children
affect mostly temporal >> frontal; cortex and extend to WM
lesion may be clearly demarcated (50%) or can be blurred
calcification in 20-36%
usually single- or multi-cystic

DNET Example

¹⁴

(A–C) T1 postgadolinium, T2-weighted coronal and axial fluid-attenuated inversion recovery images showing a dysembryoplastic neuroepithelial tumor (DNT) associated with focal cortical dysplasia (confirmed in the postoperative histopathology) in the right temporal lobe in a 23-year-old patient with refractory partial seizures since the age of 9 years, who became seizure-free after lesionectomy. Note a small area of intratumoral contrast enhancement (A: arrow), and the classic heterogeneous aspect of the tumor in all magnetic resonance imaging (sequences, sometimes given the appearance of small microcysts inside the lesion. (D–F) Coronal T2-weighted and sagittal T1-weighted images showing a DNT in the left temporal lobe in a patient with seizures since childhood who became seizure-free after lesionectomy.

Ganglioglioma

4% of pediatric CNS tumours³⁸
40% of epilepsy-associated tumours
subtype/differentiation:
- WHO grade 1 (pilocytic) astrocytoma, the most common (93%)
- WHO grade 2 (fibrillary) astrocytoma, much less common (6%)
- Rarely, malignant anaplastic WHO grade 3 (1%) or WHO grade 4 (GBM)
Gangliocytoma - purely neuronal variant

Ganglioglioma Imaging

Can present as solid mass (43%), cyst (5%), or mixed lesion (52%)³⁹
Cortically-based, hypo/iso intense to GM and hyperintense on T2

Ganglioglioma Example

Oligodendroglioma

¹⁴

Pleomorphic xanthoastrocytoma (PXA)

rare tumor in children/young adults, highly epileptogenic
glial > neuronal component
temporal (49%) > parietal/frontal/occipital⁴⁰
malignant in 20%
cortically based, classically cystic with enhancement of solid component
calcification rare, edema uncommon

Pleomorphic xanthoastrocytoma (PXA)

³⁸

Hypothalamic Hemartoma

Heterotopic developmental malformation - mixture of normal neurons and glial cells (ventral hypothalamus)⁴¹
Clinical:
- endocrine (e.g. precocious puberty)
- psychiatric (mood, behavior, “rage attacks”)
- neurological (ID, epilepsy, epileptic encephalopathy)
Seizures:
- onset usually first year
- gelastic, dialetpic, GTC

Delalande Classification of HH

⁴¹

Delalande - Imaging

⁴¹

Share All panels show coronal T2-weighted MRI. HH lesion type is designated according to the proposed classification system of Delalande and Fohlen.44 (A) Type I HH: 2-year-old boy with mild developmental delay but otherwise asymptomatic. Note attachment of the HH lesion entirely below the floor of the third ventricle. (B) Type II HH: 5-year-old boy with a history of gelastic seizures since 12 months of age. Note attachment to the left side of the hypothalamus, entirely above the floor of the third ventricle. (C) Type III HH: 31-year-old woman with refractory epilepsy, including gelastic seizures since infancy. Note attachment of the HH lesion to the right side of the hypothalamus both above and below the floor of the third ventricle. (D) Type IV HH: 3-year-old girl with severe developmental delay, history of precocious puberty, and multiple daily gelastic seizures. Type IV is designated by Delalande and Fohlen as a “giant” HH, but criteria to distinguish between types III and IV were not offered. We (Barrow Neurologic Institute) currently use a volume measurement over 8 cm3 to designate type IV, measuring the maximal length of the lesion in the 3 major axes, then utilizing the formula for determining the volume of an ellipsoid (courtesy of John F. Kerrigan, MD, Barrow Neurologic Institute).

HH imaging

¹⁴

Neurocutaneous syndromes

Tuberous sclerosis complex
Sturge Weber syndrome
Less common - hypomelanosis of Ito, epidermal nevus syndrome, Wyburn-Mason syndrome, incontinentia pigmenti

TSC

Tuberous Sclerosis Complex

⁴²

Tuberous Sclerosis Complex

Rare monogenic neurocutaneous syndrome due to mutations in TSC1 or TSC2, tumor suppressor genes in the mTOR pathway
Abnormalities on brain MRI in >95% TSC patients⁴³
4 major TSC-related manifestations on neuroimaging:

cortical tubers
white matter lesions
sub-ependymal nodules
sub-ependymal giant cell astrocytomas

More rarely, can have intra-parenchymal calcifications, hemimegalencephaly, cerebral or cerebellar malformations, intracranial aneurysms and occlusive vascular disorders.

Subcortical Tubers in TSC

Glioneuronal brain hemartomas
disrupted 6-layer organization of the cortex
usually frontal or parietal but can be spread in all lobes
Can be under-recognized in first years of life due to similarity with adjacent unmyelinated WM
Single or multiple may be dominant epileptogenic trigger

Different types of cortical tubers

type A (hyperintense on T2w and isointense on T1w)
type B (hyperintense on T2w and hypointense on T1w)
type C (hyperintense on T2w with low signal inner core and heterogeneous halo on FLAIR, hypointense on T1w, with increased diffusion on apparent diffusion coefficient maps)
with each step higher burden of FCD-like and inflammatory features
proposed - type D - similar to type C but calcified

Cortical Tuber Types

⁴³

MRI features of different tuber types. a Type A cortical tuber in the right occipital lobe of a 15-year-old female patient with TSC1 mutation showing moderate hyperintensity on TSE T2w and FLAIR images, isointensity on TFE T1w, no increased diffusion on ADC maps and no calcification on SWI. b Type B cortical tuber in the left frontal lobe of the same 15-year-old female patient with TSC1 mutation showing hyperintensity on TSE T2w and FLAIR images with corresponding hypointensity on T1w IR, no increased diffusion on ADC maps and no calcification on SWI. c Type C cortical tuber in the left parietal lobe of a 12-year-old male patient with TSC2 mutation showing hyperintensity on TSE T2w and FLAIR images with corresponding hypointensity on TFE T1w, increased diffusion on ADC maps but no calcification on SWI. d Largely calcified cortical tuber (also named type D) in the right temporalparietal lobe of a 6-year-old female patient with TSC2 mutation showing hypointense inner core with hyperintense halo on TSE T2w and FLAIR images, mild hyperintensity on SE T1w, signal drop on ADC maps and marked hypointensity on GRE due to calcified components

Radial migration lines

⁴³

Sub-ependymal nodules

⁴³

Subependymal giant cell astrocytomas (SEGA)

WHO grade I astrocytoma
15- 25% TSC patients,
More common with TSC2 than TSC1
MRI every 1–3 years for SEGA screening (2012 Tuberous Sclerosis Alliance Consensus)
Asymptomatic/incidental - hydrocephalus

Subependymal giant cell astrocytomas (SEGA)

Sub-ependymal giant cell astrocytoma in a 13-year-old female patient with TSC2 mutation. Axial non-contrast computed tomography performed at emergency department (a) showed an inhomogeneous partially calcified soft tissue mass abutting in the left lateral ventricle, with hypodense peripheral halo within frontal lobe parenchyma and associated bilateral hydrocephalus. On MRI, axial T2w (b) and axial FLAIR (c) images demonstrated the presence of a lobulated mass with inner cystic components, causing oedema and trapping of the frontal horn (asterisk); axial GRE (d) also confirmed calcifications of the implant site on lateral left ventricle wall (black arrowhead); the lesion presented with intermediate ADC values (e), inhomogeneous T1w signal (f) and intense contrast enhancement of solid components (g, h). On coronal plan, biventricular hydrocephalus is expl

Sturge Weber syndrome

Leptomeningeal angiomatosis
Rare neurocutaneous disorder
Epilepsy (75-90%), progressive developmental delay, facial telangiectatic nevi
Pathogenesis thought be related to vascular steal
May be associated with pathogenic variants in GNAQ - sporadic

Sturge Weber Imaging

Radiopedia, case 84666

Sturge Weber Imaging

³⁷

Sturge Weber Imaging

Radiopedia, case 84666

Objectives

Imaging basics and modalities
Review indications for neuroimaging in pediatric epilepsy
Imaging guidelines suggested by ILAE
Overview of common and less common substrates for epilepsy

Thank you

Additional Reading

MR Physics and Sequences
- Questions and Answers in MRI
- Introduction to Magnetic Resonance Imaging for Neurologists
Overview of imaging
- Neuroimaging in Pediatric Epilepsy: A Multimodality Approach
Myelination patterns
- Normal myelination

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Neuroimaging in Pediatric Epilepsy

Discolosures

Objectives

Neuroimaging basics

What modalities are available?

WHAT are we actually measuring with MRI?

MRI Physics Primer

“Relaxation”

T1 vs T2

Signal Detection

MR Sequences

WHY is imaging important in epilepsy?

Reasons for Neuroimaging

Lesional vs Non-lesional epilepsy

Finding a lesion may completely change your approach!

WHEN should we image?

Indications for Structural Neuroimaging5

What is the yield of imaging?

HOW to perform MRI in patients with epilepsy?

Recommended protocol

HARNESS-MRI

HARNESS-MRI

HARNESS-MRI Advantatges

Overview of imaging findings in pediatric epilepsy

Overview

Malformations of Cortical Development

The human brain is a clonal mosaic

Timing is everything…

Focal Cortical Dysplasia (FCD)

FCD Classification

Classification Update

FCD Histology

FCD Imaging - General Features

Where is the lesion?

Voxel-Based Morphometry

Type 1 FCD

Type 1 FCD

Type 1 FCD

Type 2 FCD

Type 2 FCD

FCD2A

Bottom of Sulcus Dysplasia

Transmantle sign in FCD IIb

Black Line Sign in FCD IIB

Type 3 FCD

Type 3 FCD

MOGHE

Mild malformation of cortical development with oligodendroglial hyperplasia in epilepsy

MOGHE Imaging Features

MOGHE Imaging Features

Hemimegalencephaly

Hemimegalencephaly

Hemimegalencephaly - Imaging

Total Hemimegalencephaly

Other MCD

Polymicrogyria (PMG)

Bilateral PeriSylvian Syndrome

Bilateral Peri-Sylvian PMG

PMG Spectrum

Schizencephaly

Periventricular nodular heterotopia (PVNH)

Periventricular nodular heterotopia (PVNH)

Subcortical band heterotopia (double cortex)

Subcortical band heterotopia (double cortex)

Perinatal Insults

A note about timing…

Myelination Progression

Hypoxic-ischemic encephalopathy (HIE)

HIE Injury Patterns

Sequalae of HIE

Sequalae of HIE

Sequalae of HIE

Perinatal arterial ischemic stroke

Epilepsy after perinatal injury

Mesial Temporal Sclerosis (MTS)

MTS Imaging

MTS

Adult vs Pediatric MTS

Rasmussen Encephalitis

Rasmussen Encephalitis

Indications for Structural Neuroimaging⁵