Epilepsy

TOPIC REVIEW
Imaging in Epilepsy
Pongsakorn O. MD.
Advisor Assoc. Prof Sukulaya L. Radiologist
Seizure
oParoxyamal alteration in neurologic function resulting from
abnormal, excessive neural activity.
oLoss of normal regulation of neuronal excitation and
inhibition.
Epilepsy
oChronic condition characterized by recurrent seizures
without any systemic cause.
oNot indicate specific pathology.
oRequires long term medial treatment or surgery.
Seizure and Epilepsy

oAll patients with epilepsy experience seizures, not all
individuals with seizures have epilepsy.

Simple partial
Remain conscious
Partial seizure
Focal onset seizure
Generalized seizure
Tonic clonic seizure
with unconsciousness
Complex partial
Lose conscious
Secondarily generalized seizure
Seizures
Epilepsy
oDiagnosis of epilepsy of epilepsy involves four key stages
o Recognition of epileptic seizures.
o Classification of the seizure type(s).
o Identification of the epilepsy syndrome.
o Identification of an underlying etiology.
Imaging in epilepsy: a paediatric perspective, BrJR, 74 (2001).

First seizure
4% of population
Epilepsy
1% of population
Uncontrollable
seizure
0.4% of population
80% has epileptogenic focus
detected on MRI
Epilepsy
http://www.ilae.org/Visitors/Centre/ctf/documents/ILAEHandoutV10_000.pdf
Epilepsy
oIn uncontrollable epilepsy patient, is there any brain
morphological abnormality?
oNeuroimaging plays important role in
o To assist in identifying the epilepsy syndrome.
o To identify any underlying etiology.
o Facilitate a prognosis
o Provide genetic counselling advice
Epilepsy
oNot every child with epilepsy needs brain imaging.
oWho require imaging (children patient)
o Focal neurological deficit/asymmetry
o Neuro-cutaneous syndromes
o Developmental refression
o Simple partial seizures
o Refactory complex partial seizures
o Children with infantile spasms/myoclonic seizures in first year
Epilepsy
o Who do not require imaging (children patient)
o Primary (idiopathic) generalized seizures
o Petit mal seizures
o Juvenile myoclonic seizures
o Grand mal epilepsy
o Benign partial seizures with centrotemporal or occipital spikes

o Simple febrile convulsions
o Focal discharge on single EEG
Epilepsy
http://www.radiologyassistant.nl/en/p4f53597deae16/role-of-mri-in-epilepsy.html.
Imaging
oStructural studies
o CT
o MRI
oFunctional studies
o Functional MRI
o Nuclear study
CT scan
o Emergency setting (status epilepticus, trauma)
o Initial evaluation of seizures presenting with focal neuro deficit,
fever
o Calcification in Sturge-Weber
o Useful as a screening tool
MRI
o Anatomical characterization
o Identify and localize the structural abnormality
o Identification of the surgical candidates
o Surgical planning
o Relationship between surgical target and functionally important
brain areas
MR Epilepsy protocol
o Field magnet should be at least 1.5 T.
o Main objective - to achieve maximum tissue contrast between gray
and white matter with high spatial resolution.
o 3 T magnets have the more advantage than 1.5 T.
o increasing the signalto-noise ratio (resolution) and improving image contrast
in T2.
o allows for high-resolution matrices (of up to 1024) in T2 sequences
o decrease of section thickness to 1-2 mm in 2D sequences and to 0.7 mm in
3D sequences
o Used in patient with refractory epilepsy with negative or nonconclusive
findings from 1.5 T MR system.
Structural magnetic resonance imaging in epilepsy, Radiologa. 2012;54(1):9-20
High-resolution T2 (A) 3D-T1 (B) images obtained with a 3 T magnet. High spatial and contrast
resolution allow a more detailed assessment of the cortex and gray---white matter junction.
o T1-weighted sequences in 3D mode, with isotropic voxel of 1 mm,
including the whole brain (allow reconstruction without losing
image quality).
o Inversion-recovery prepared gradient echo (GE) pulse sequences
are used to increase gray and white matter contrast.
o Coronal high-resolution T2-weighted sequences (3 mm thickness)
perpendicular to the hippocampus
o Hippocampus should always be evaluated even electroclinical data are not
suggestive of temporal lobe epilepsy
o FLAIR sequences in the same planes should also be used to detect

contrast changes in the hippocampus (3-4 mm thickness).
o More sensitive for the detection of small signal changes than T2 sequences,
especially adjacent to the cerebrospinal fluid
T2
FLAIR
Probable focal cortical dysplasia : T2 (A) and FLAIR (B) sequences. The small juxtacortical lesion
is more clearly visible on the FLAIR sequence.
o Axial T2*, either standard GE technique or echo-planar imaging
(EPI) for detection of magnetic susceptibility (4-5 mm thickness)
o Because fast-SE technique - low sensitivity to magnetic susceptibility, lesions
containing calcification or hemosiderin such as cavernomas may not detected
T2-FSE
T2-EPI
T2-FSE (A) and T2-EPI (B) sequences. The small left parietal cavernoma is visible on T2-EPI but
undetected on T2-FSE.
o Moreover, even if a temporal origin is highly suspected, axial FLAIR
sequences (alternatively T2) should be performed.
o to rule out small lesions that directly cause the seizure, or lesions associated
with an hippocampal abnormality (dual pathology)
o Postcontrast sequences are not indicated in a basic epilepsy
protocol, unless suspected of a specific lesion, particularly brain
tumor.
Sequence
T1WI
Description
Isotropic 3D sequence
T2WI and/or FLAIR Coronal perpendicular to hippocampus

FLAIR
Axial whole brain
T2* or SWI
Axial whole brain
CE T1WI
Additional for specific lesion
Epilepsy protocol
- Coronal 3D reformatted T1
weighted image (A),
- Coronal T2 sequences (B)
- FLAIR images sequences (C),
- Axial FLAIR sequences (D)
- Axial T2-EPI sequences (E)
Epilepsy
Temporal lobe
o Anatomy of temporal lobe
o Lies inferior to the sylvian fissure
o Lateral surface 3 gyri
o Superior temporal gyrus
o Middle temporal gyrus
o Inferior temporal gyrus
Temporal lobe Limbic system

o Temporal lobe contains major subdivision of limbic system
o Limbic lobe
o Composed of
o subcallosal, cingulate, parahipocampal gyri.
o Hippocampus, subiculum, .dentate gyrus, entorhinal cortex
o Limbic system
o Limbic lobe + some subcortical structure : eg. amygdala, mammillary
bodies, septal nuclei, etc
Diagnostic and surgical imaging anatomy : brain, head and neck, spine

o Limbic lobe formed by 3 C-shape arches
surrounding diencephalon, basal ganglia

o Outer arch (Blue)
o From temporal lobe to frontal lobe
o Composed of
o Unchus (anterior end of parahippocampal gyrus
o Parahippocampal gyrus
o Cingulate gyrus
o Subcallosal area

o Middle arch (Yellow)
o From temporal lobe to frontal lobe
o Composed of
o Hippocampal proper (Ammon horn).
o Dentate gyrus.
o Supracallosal gyrus (indusium griseum).
o Paraterminal gyrus.

o Inner arch (Purple)
o From temporal lobe to mammillary bodies
o Composed of
o Fornix
o Fimbria
Limbic system - Hippocampus

o Hippocampus lies on medial aspect of temporal
horn bulges into its floor.
o Hippocampus means Seahorse

o Hippocampus has 3 anatomic segments
o Head (pes hippocampus) : digitated anterior part.
o Body : cylindrical
o Tail : narrowed and curves around the corpus
callosum splenium
Head
Tail
Body
Osborns brain : imaging, pathology and anatomy, 1st edition

o Hippocampus composed of 2 interlocking
U-shaped of gray matter
o Ammon horn (Cornu ammonis = CA)
o Superolateral, upside-down U
Ammon horn
o Dentate gyrus
o Inferomedial U
Dentate gyrus

o Ammon horn subdivided into 4 zones, based on
width, cell size, and cell density
o CA1
o lateral, outermost zone
o vulnerable to anoxia
o CA2
o Curves superomedially from CA1
o relatively resistant to anoxia
o CA3
o Loose band, merged into CA4
o CA4
o innermost zone
o enveloped by dentate gyrus
Temporal lobe Imaging anatomy

o Superior, middle and inferior temporal gyri best seen on sagittal
scans
o Hippocampus best seen on coronal scans, perpendicular to long
axis of hippocampus

o Coronal scan of hippocampus : seahorse-shaped structure below
the choroid fissure and temporal horn of lateral ventricle
High resolution coronal T2WI


o Parahippocampal gyrus is separated from dentate gyrus by
hippocampal sulcus. The collateral sulcus is landmark, lie
inferolateral to parahippocampal gyrus
High resolution coronal T2WI
Mesial Temporal Sclerosis (MTS)

o Most common overall localization-related form of epilepsy.
o Most common manifestation is complex partial seizure.
o Occur in older children and young adult, no gender predominance.
o Etiology
o Variety of events such as trauma, febrile seizure or infection before age of 5,
and the end result is MTS.
o Unclear, but inflammatory process or prolonged seizures with hippocampal
hypoxic-ischemic injury is considered.
o 8-22% associated with another epileptogenic cause (dual pathology) less
favorable surgical outcome
o most common : focal cortical dysplasia
Imaging of the brain, chapter 50: epilepsy, 1st edition
Coronal T2WI
a 27-year-old man with history of
epilepsy and head trauma
- Temporal lobe encephalomalacia
- Shrunken hippocampus
- hyperintense hippocampus
Consistent with MTS.
Dual Pathology
Mesial temporal sclerosis with a hyperintense and shrunken hippocampus, and secondary
enlargement of the left temporal horn
Associated subcortical hyperintensity in the left temporal lobe indicating focal cortical dysplasia.

o Pathology
o Atrophy of hippocampus and adjacent structures esp hippocampal
body (80-90%)
o 15-20% bilateral but usually asymmetrical
o Neural loss and astrogliosis is typical histologic findings
Coronal graphic of typical MTS

- Atrophy hippocampus
- Sclerotic with loss of normal
internal architecture
- Enlarged temporal horn
- Small ipsilateral fornix

o Presentation
o Complex partial seizure
o May preceding with aura fear, anxiety, automatic symptom

o Imaging
1) MR findings
- Found in 60-70% of TLE
- T1WI
- Atrophy hippocampus and associated with atrophy of ipsilateral thalamus, fornix and
mammillary body
- Loss of hippocampal head digitation
- Widening of adjacent temporal horn + choroid fissure
- T2/FLAIR : Hyperintensity with obscuration of hippocampal architecture on

- Hyperintensity on DWI and increased diffusivity on ADC (T2 shine through)
- No contrast enhancement
- Reduced NAA (neural loss), unchanged Cho and Cr
A 37-year-old woman with temporal lobe epilepsy
Coronal true inversion recovery scan
Coronal thin-section T2WI
Shrunken left hippocampus
Hyperintensity of shrunken left hippocampus
Small ipsilateral fornix
mildly enlarged temporal horn is


o Imaging
2) Nuclear Medicine findings
- Most sensitive for diagnosis MTS
- Temporal lobe hypometabolism : most typical finding
- Epileptogenic zone : hyperfperusion in ictal phase
: hypoperfusion in interictal phase
Sagittal and coronal FDG PET scan marked hypometabolism in entire left temporal lobe

o Imaging
2) Nuclear Medicine findings
- Most sensitive for diagnosis MTS
- Temporal lobe hypometabolism : most typical finding
- Epileptogenic zone : hyperfperusion in ictal phase
: hypoperfusion in interictal phase

o Hippocampal volumetry
o Criteria set forth by Watson and coworkers in 1992.
o For define anatomic boundaries to measure volume of hippocampus
and amygdala
o Each center need to establish normative data
Anatomic basis of amygdaloid and hippocampal volume measurement by magnetic resonance imaging,
Neurology, 1992 Sep;42(9):1743-50.

o Hippocampal volumetry
o Recent study show quantitative MR (volumetry) imaging depict the
presence and laterality of HA in TLE with accuracy rates that may
exceed visual inspection of clinical MR imaging studies
Temporal Lobe Epilepsy: Quantitative MR Volumetry in Detection of Hippocampal Atrophy,

Radiology: Volume 264: Number 2August 2012.

o Diagnosis
o Based on concordance of clinical, electroencephalographic and
imaging data

o Differential diagnosis hyperintense lesion on T2/FLAIR
1) Status epilepticus
o T2/FLAIR : Hyperintensity and/or enhancement in affected cortex as well as
hippocampus
o DWI : Diffusion restriction due to cytotoxic edema in the acute stage.
2) Low-grade glioma
o WHO grade II : astrocytoma, oligodendroglioma, oligoastrocytoma
o T2/FLAIR : Hyperintensity
o Mass effect not volume loss
Status epilepticus
T2/FLAIR : Hyperintense hippocampus, but there is edema with a slightly compressed
temporal horn (no atrophy).
DWI : diffusion restriction due to cytotoxic edema in the acute stage.

o Differential diagnosis hyperintense lesion on T2/FLAIR
3) Cortical based neoplasm
o dysembryoplastic neuroepithlial tumor (DNET)
o Well-demarcated, bubbly mass with often associated cortical dysplasia
4) Cortical dysplasia
o Isointense of gray matter but T2 hyperintense in underlying white matter
NO SIGN OF VOLUME LOSS !!!
DysEmbryoplastic Neuroepithelial Tumor (DNET)

Hyperintense but enlarged hippocampus with a bubbly appearance.

o Treatment
o Anteromedial temporal lobectomy : successful in 70-90% of drugresistant TLE.
Epilepsy
Malformation of Cortical Development

(MCDs)

(MCDs)
o Broad spectrum of cortical lesion resulting from deranged
developmental process and formation of the cortical mantle
o 3 stages of cortical development
o Proliferation
o Neural migration
o Post-migration development

(MCDs)
o Barkovich et al classify MCDs depend on which development stages
is affected
o Group I : Abnormal of neuronal and glial proliferation or apoptosis
o Resulting in too many or too few cell

(MCDs)
is affected
o Group II : Abnormal of neuronal migration

(MCDs)
is affected
o Group III : Abnormalities of post-migrational development
o Associated with prenatal and perinatal insult
MCDs Abnormal cell numbers/type

o Focal Cortical Dysplasia (FCD)
o Microcephalies (MCPH)
o Hemimegaloencephaly (HMEG)

Focal Cortical Dysplasia (FCD)

o Common cause of medically refractory epilepsy
o Localized regions of non-neoplastic malformation of gray matter
o FCD type II is most common (isolated lesion with altered cortical
layering and dysmorphic neurons without or with balloon cells)
o Cause of epilepsy in children and young adults
o 15-20% of patients undergoing epilepsy surgery
o Outcome of surgical resection varies depend on subtype, seizure
control 70-100% in FCD type IIb

o Imaging
o Often subtle , smaller than 2 cm.
o CT finding
o Usually normal, unless the lesion is unusually large

o MRI finding - Depend on lesion type and subtype
o FCD type IIb
o localized area of increased cortical thickness and funnel-shaped area of blurred gray-white
interface at the bottom of sulcus, transmantle MR sign
o SI varies with age :
o In neonate and infant high SI on T1 and mildly low SI on T2
o In older patient high SI on T2/FLAIR
o No enhancement
o DWI : Increased diffusivity
o MRS : decreased NAA:Cr, elevated mI
o Perfusion MR : normal or reduced rCBV
o Ictal SPECT, PET can be useful in patient with normal MRI and suspected FCD
T2WI in 17-year-old female with

seizures
- right frontal wedge-shaped
area of malformed cortex
- Biopsy : focal cortical dysplasia
IIb (classic Taylor FCD, the most
common type)
FCD type II in a 10-month-old boy with

congenital epilepsy.
(a) Axial T2WI
- focal cortical thickening of the gray matter in
the right parietal region
(b) Axial T1WI
- blurring of the gray matterwhite matter
junction
(c) Axial DTI
- thin splenium, suggests hypomyelination.
(d) Interictal MR/FDG-PET fusion
- large area of hypometabolic activity
Neuroimaging in Pediatric Epilepsy: A Multimodality Approach, RadioGraphics 2008; 28:10791095

Microcephalies (MCPH)
o = small head, head circumference < 3 SD for age
o Cause can be primary (genetic) and secondary (non-genentic)
o 3 types of primary microcephalies
o Microcephaly with simplified gyral pattern (MSG)
o Microlissencephaly
o microcephaly with extensive polymicrogyria
Microcephaly with simplified gyral pattern
Microcephaly with polymicrogyria
Microcephaly with lissencephaly
o Presents with mental retardation, developmental delay and seizure
o Imaging
o Decreased craniofacial ratio (usually < 1.5 : 1)
o Slanted forehead
o Overriding calvarial suture
o CT findings
o Small cranial vault with closely apposed and overriding sutures
o In older children : thicken skull and hyperpneumatized sinus
o MRI findings
o Small brain but relatively normal.
o In microcephaly with simplified gyral pattern : shallow sulci (25-50% of
normal)
o Delayed myelin mile stone
o Associated with callosal dysgenesis and cephaloceles
dysplastic
corpus callosum
sloping forehead
Primary microcephaly
Sagittal T1WI
Axial T2WI
- Craniofacial disproportion (1.5:1)
- Simplified gyral pattern with too few

gyri
- sloping forehead
- thin dysplastic corpus callosum
- Simplified gyral pattern
- Shallow appearing sulci

- Disproportionately large eyes
Primary microcephaly
Axial T2WI
- Simplified gyral pattern with numerous shallow sulci.
- Normal cortical thickness, but delayed myelination.

Hemimegalocephaly (HMEG)
o Unilateral megalencephaly enlargement of one cerebral
hemisphere
o Rare, < 5% of MCDs
o Usually present symptoms in infancy
o Macrocania
o Developmental delay
o Seizure
o Unilateral motor deficit
o Extracranial hemihypertrophy of ipsilateral body
o Imaging
o Enlarged, dysplastic appearing hemisphere with abnormal gyration,
thickened cortex and white matter abnormalities
o CT findings
o NECT
o Enlarge hemisphere and hemicranium
o Abnormal increased attenuation of white matter of affected hemisphere due to
abnormal myelination --> relative hypodense of normal side white matter
o CECT
o Abnormal uncondensed primitive superficial vein over dysplastic cortex.
o MR findings
o T1WI
o Thickened and lumpy-bumpy cortex.
o Enlarged ipsilateral ventricle.
o T2WI
o Patchy and polymicrogyria with indistrict gray-white junction
o Heterogeneous with cysts and gliosis-like Hyperintensity
o DTI and fiber tractography

o Asymmetrically increased anisotropic movement of water molecules, representing
hypermyelination
A 4-year-old girl with hemimegaloencephaly and intractable seizures
NECT
T2WI
- Enlarged right hemisphere and hemicranium
- Enlarged hemisphere
- Enlarged WM in the corona radiate, compared

with normal WM of the left-side hemisphere
- Hyperintense WM
- Enlarged deformed lateral ventricle
- Thickened dysplastic cortex
Right hemimegalencephaly in a patient with

intractable epilepsy
(a) Axial T2WI
- Pachygyria and right cortical thickening
- Abnormal hypointensity of the subjacent white
matter
(b) Axial DTI : Hypermyelination in the white
matter of the right anterior frontal lobe
(c) Tractography : Abundant fibers in the right
hemisphere than on the normal left side.
(d) Axial ictal MR/FDG-PET fusion image : Area
of hypermetabolic activity in the cortex of right
frontal lobe.
Neuroimaging in Pediatric Epilepsy: A Multimodality Approach, RadioGraphics 2008; 28:10791095
MCDs Abnormal cell migration

o Heterotopias
o Lissencephaly spectrum
o Subcortical heterotropias and lobar dysplasia
o Cubblestone malformations

o Heterotopias
Heterotopias
o Arrest of normal neuronal migration, result in collection of
heterotopic gray matter anywhere between ventricle and pia
o Periventricular nodular heterotopia (PVNH) : most common form
of adult cortical malformation
o Subependymal nodules of gray matter line lateral wall of lateral
ventricles follow SI of GM, no enhancement
o dDx with subependymal nodules of tuberous sclerosis : no calcified,
overlying cortex appears thinned but sulcation and gyration normal
Axial T2WI in a patient with corpus callosum agenesis
- Multiple nodules of subependymal heterotopic gray matter

- Pachy- and polymicrogyria at perisylvian cortical areas
- Heterotopias followed gray matter signal intensity on all sequences
Nodular gray matter heterotopia versus Tuberous sclerosis.
Coronal SPGR MR
- Small bilateral subependymal
lesions following the signal of
gray matter
Axial T2WI
- Multiple small, focal periventricular lesions that are
isointense to cortex, followed the signal of gray matter on
all sequences
- Consistent with foci of nodular heterotopic gray matter

Nodular gray matter heterotopia versus Tuberous sclerosis.
Coronal T2WI of 4 month-old patient
Coronal T1WI
- areas of T2 hypointensity within the subcortical

white matter and subependymal location of
lateral ventricle.
- multiple areas of hyperintensity within the

subcortical, deep white matter and subependymal
area of lateral ventricle.
- these areas of hyperintensity do not match the

signal of gray matter, suspected tuberous sclerosis

o Heterotopias
Lissencephaly spectrum
o Smooth brain, brain surface lacks of normal sulcation and gyration
o Abnormal transmental migration include
o Agyria : thick cortex with absence of surface gyri
o Pachygyria : board flat gyri
o Band heterotopia (double cortex syndrome) : mildest form of classic
lissencephaly
o Presents with developmental delay, impaired neuromotor functions,

mental retardation and seizure
o Associated with severe facial deformities --> Miller-Dieker syndrome
o Imaging in complete classic Lissencephaly
o Smooth, featureless brain surface
o Shallow sylvian fissure
o Large ventricles
o Thick cortex with diminished WM
o Loss of interdigitation between gray and white matter
o Hypoplastic cerebellum in some case
o CT findings
o NECT
o On axial : hourglass or figure of eight appearance flat brain surface with
shallow, wide sylvian fissures
o Thick dense cortex surround thinner, smooth band of white matter
o CECT
o Prominent primitive-appearing veins running into shallow sylvian fissures and
coursing over thickened cortices
o MR findings (classic Lissencephaly)
o T1WI
o Smooth cortical surface
o thick band of deep gray matter which sharply demarcated from underlying white
matter
o Large ventricle
o Callosal hypogenesis : thin, flat body with more upslanted splenium
o T2WI
o Separate cortical layers : thin outer cellular layer (isodense with GM) covers
hyperintense cell-sparse layer and deeper thick layers arrested neuron
o Smooth WM layer but reduced in volume
o MR findings (classic Lissencephaly)
o DTI
o Pruning, rarefaction, and disorganization of subcortical association (U)
fibers
o Main WM tracts also appear aberrant and heterotopic
A 4- month-old girl with classic lissencephaly
NECT
- Smooth, nearly agyric surface with shallow
sylvian fissures : hourglass configuration.
hypointense
cell-sparse layer
T1WI
- Few shallow sulci with broad flat gyri
- Thick cortex with reduced white matter
- Thin outer, thick inner layers of GM, separated

by a hypointense cell-sparse layer
- Moderately enlarged ventricles
- Reduced WM volume
Thin outer cortex

hyperintense
cell-sparse layer
thickened inner band

of GM
Coronal T2WI
DTI shows
- Thin smooth outer cortex with hyperintense

cell-sparse layer and markedly thickened inner
band of GM
- Absence of arborized subcortical U-fibers
- Disorganized major WM tracts (multidirectional

encoded color bands)
- Primitive-appearing cortical veins in shallow

sylvian fissures
Lissencephaly Band heterotopias

o Double cortex syndrome
o Band of smooth GM separated from relatively thicker, more gyriform
cortex by a layer of normal-appearing white matter.
o Distinguishing feature : homogeneous layer of gray matter

separated from the ventricles and cerebral cortex by normalappearing WM --> double cortex
Axial T2WI
Coronal SPGR
- Subcortical bands follow GM signal intensity

with thin overlying cortex
- Bilateral homogeneous-appearing bands of

subcortical heterotopic gray matter
MCDs
Abnormal post-migrational development
o Polymicrogyria (PMG)
o Schizencephaly
MCDs
o Schizencephaly
Polymicrogyria (PMG)
o Irregular cortex with numerous small convolutions and shallow or
obliterated sulci --> lumpy-bumpy appearance
o Both genetic and none-genetic (TORCH infection, intrauterine
vascular accident, trauma and metabolic disorder) causes.
o Most common location : bilateral perisylvian (61%)
o Associated with periventricular GM heterotopias (11%), other
anomalies such as schizencephaly.
o Presents at any age
o Symptoms depend on location
o Developmental delay
o Focal neurological deficit
o Seizure
o Imaging
o MR procedure of choice
o Thickened or overfolded cortex with nodular surface
o Irregular stippled gray-white matter interface
Both pachy- and polymicrogyria

- several foci of tiny nodules (gyri piled
on top of gyri) giving the brain surface an
irregular pebbly appearance.
Axial T2WI in a 2-week-old infant with seizures
Coronal T2WI
- Multiple foci of polymicrogyria, more

prominent on the left side
- Appearance of multiple tiny nodules of gray

matter piled on top of gyri, polymicrogyria
MCDs
o Schizencephaly
Schizencephaly
o = Spit brain
o Gray matter line cleft from ventricular ependymal to pial surface of
the cortex
o Lip of the cleft : 2 types

o Fused or closely apposed lip Closed lip schizencephaly
o Widely apposed lip Open lip schizencephaly
o Presentation : drug-resistant epilepsy, developmental delay and

motor impairment
Schizencephaly
o Imaging - key imaging features
o (1) CSF-filling defect extending from the ventricle to pial surface
o (2) dysplastic gray matter lining the cleft
o NECT
o Focal outpouching of CSF from lateral ventricle
o 60% unilateral and 40% bilateral
o Relatively hyperdense cortex lining the cleft
o Common associated with absent septum pellucidum (70% of case) and
thin or dysplastic corpus callosum
Schizencephaly
o MR findings
o More sensitive than CT, esp detect associated findings : cortical
dysplasia (polymicrogyria, pachygyria) and heterotopic gray matter
o Cleft followed CSF in all sequence

o CTA/MRA detects occlusion or absence of MCA in some case
Cleft
Outpouching CSF
NECT in a 19-yearold man with unilateral schizencephaly

- Outpouching of CSF from the lateral ventricle and continuous with a
thin seam of CSF that extends to the surface of the hemisphere
- Dysplastic appearing GM lining the cleft
- Dysplastic GM extending to ventricular ependyma
Sagittal T1WI
Axial FLAIR scan
- Large CSF-filled cleft extending superiorly

from the lateral ventricle.
- Bilateral schizencephalic clefts, lining with

dysplastic GM
- Cleft is lined with dysplastic-appearing gray

matter.
- Clefts is suppressed completely on FLAIR

Sagittal T1WI and T2WI Unilateral closed lip schizencephaly
- Gray matter extending from the ventricle to the pial surface of the brain.
- Gray matter lining the cleft is the same signal intensity as the cortex.
Epilepsy
Epileptogenic tumors
o Ganglioglioma
o Dysembryoplastic neuroepithelial tumor (DNET)
o Low-grade diffuse astrocytoma
o Hypothalamic hamartoma
o Other
o Pilocytic astrocytoma
o Pleomorphic xanthroastrocytoma
o Oligodendroglioma
Temporal lobe epilepsy

o Most common = mesial temporal sclerosis
o Tumor associated temporal lobe epilepsy
o Ganglioglioma (40%)
o Dysembryoplastic neuroepithelial tumor (DNET) (20%)
o Low-grade diffuse astrocytoma (20%)
o Other (20%)
o Oligodendroglioma
o Ganglioglioma
o Other
o Oligodendroglioma
Ganglioglioma
o WHO grade I
o 1-1.5% of all primary brain tumor but more common in children (510% of pediatric CNS neoplasm)
o Well-differentiated, slow growing tumor, composed of dysplastic

ganglion cell and neoplastic glial cell.
o Usually solitary lesion, occur throughout the CNS including spinal cord
o 75% in temporal lobe
o 15% in posterior fossa esp brain stem or cerebellum
o 10% in frontal lobe
Ganglioglioma
o Cortical based superficial lesoion and often expand the cortex
o 2 general patterns
o Cyst with mural nodule
o Solid tumor
o Calcification is common but hemorrhage and necrosis are rare

o Never metastasize
o Presentation : chronic resistant temporal lobe epilepsy (90% of cases)
o Treatment : complete resection --> seizure free (80%)
Ganglioglioma
o Imaging Classic pattern : cystic mass with enhancing mural nodule
o CT finding
o Cystic component (60%) and hypodense cyst with isodense mural nodule (30%)
o 30-50% calcify
o 50% of lesion enhance following contrast admnistation
o MR findings
o Hypo to isointense on T1WI and hyperintense on T2WI/FLAIR
o Absent surrounding edema
o Enhancement varies from none, minimal to moderate but heterogeneous,
homogeneous solid enhancement also seen
Coronal MR scans in a 16-year-old boy with

longstanding seizures
- A partially cystic, partially solid left temporal
lobe mass with T2WI/FLAIR hyperintensity
nodule with ring enhancement around cyst.
Ganglioglioma, mostly solid mass in frontal

cortical/subcortical area
- T1 hypointense
- T2 hyperintense
- intense enhancement
o Ganglioglioma
o Other
o Oligodendroglioma
Dysembryogenic neuroepithelial tumor

(DNET)
o WHO grade I
o Benign, cortically base lesion with multicystic, multinodular architecture
o Often associated with cortical dysplasia
o 45-50% at temporal lobe and one third in frontal lobe

o Usually solitary lesion
o Slow growth and rare malignant transformation

(DNET)
o Common in children and young adult
o Presents with pharmacologically resistant complex partial seizure
o Treatment : lesionectomy with epilaeptogenically area around the
tumor (due to associated with cortical dysplasia) --> increased seizure
free outcome

(DNET)
o Imaging
o Well-demarcated, triangular, bubbly cortical/subcortical mass in young
patient with long-standing complex partial epilepsy
o CT findings
o Hypodense cortical/subcortical mass
o 20% calcification
o Focal bony scalloping or calvarial remodeling is common

(DNET)
o MR findings
o T1WI : multilobulated, hypointense, bubbly cortical/subcortical mass
o T2WI : strikingly hyperintense multicystic appearance
o FLAIR : hyperintense with more hyperintense rim at tumor periphery (75%
of case)
o T2* : blooming related to calcification
o Little or minimal contrast enhancement
Coronal T2WI
- A cortically based, bubbly mass with the
typical appearance of a DNET.
Sagittal T1WI
Sagittal T1WI



matter.

matter.
o Ganglioglioma
o Other
o Oligodendroglioma
Low-grade diffuse astrocytoma

o WHO grade II
o Slow growth but tendency for malignant progression to anaplastic
astrocytoma and GBM
o Location
o Nearly two third in supratentorial esp cerebral hemisphere : equally
between frontal and temporal lobe
o One third in infratentorial
o But account for 50% of brain stem tumor in children
o Occur at all age

o Presentation depend on location, most common is seizure
o Median survival of 6-10 years and recurrence after resection is common
o Most tumor progresses to higher grade within 10 years

o Imaging
o Infiltrating lesion with ill-defined boarder
o Enlargement and distortion of structure
o Blurred gray-white interface
o CT findings
o Ill-defined homogeenous mass
o Hypointense relative to white matter
o 20% calcification, but hemorrhage and cystic change are rare
o No enhancement

o Imaging
o Infiltrating lesion with ill-defined boarder
o Enlargement and distortion of structure
o Blurred gray-white interface
o CT findings
o Ill-defined homogeenous mass
o Hypointense relative to white matter
o 20% calcification, but hemorrhage and cystic change are rare
o No enhancement

o MR findings
o Moderate mass effect with adjacent cortical expansion
o Circumscribed on MRI
o T1WI : hypointense
o T2WI/FLAIR : hyperintense
o No enhancement
o DWI : no restriction
T1WI in a 37 yo man with seizures
T2WI
T1 C+ scan
- Homogeneously hypointense left - Heterogeneously hyperintense mass - No enhancement

medial temporal lobe mass in cortex
and subcortical WM
Diffusely infiltrating astrocytoma, WHO grade II

o Ganglioglioma
o Other
o Oligodendroglioma
Hypothalamic hamartoma
o Non-neoplastic congenital malformation associated with
o Precocious puberty
o Behavioral change
o Gelastic seizure (ictal laughing fits)
o Located in the tuber cinereum

o Solitary lesion
o 2 forms of hypothalamic hamartoma
o Pedunculated type attached to tuber cinereum and project in ro
suprasellar cistern
o Sessile type attatched to floor of 3rd ventricle and project to its lumen
o Imaging
o Non-enhanceing hypothalamic mass between infundibular stalk and
mammillary bodies
o CT findings
o Homogeneous suprasellar mass
o iso to slightly hypodense mass compared to brain parenchyma
o No enhancement
o Intralesional cyst may found in large lesion
o MR findings
o T1WI : isointense to normal gray matter
o T2WI/FLAIR : Slightly hyperintense
o No enhancement
mammillary bodies
hamartoma
infundibular stalk
Sagittal T2WI in a 12-month-old child with central

precocious puberty
- pedunculated hypothalamic hamartoma between
the infundibular stalk and the mammillary bodies.
Sagittal T1 C+
- no enhancement of hypothalamic
hamartoma.
- isointense with gray matter.
Floor of 3rd ventricle

hamartoma
hamartoma
mammillary bodies
infundibular stalk
Sagittal T2WI
Sagittal T2WI
- Sessile HH bulging into the floor of the third

ventricle
- tiny sessile HH just behind the infundibulum

and in front of the mammillary bodies
Epilepsy
Neurocutaneous syndrome
o Sturge-Weber syndrome
o Tuberous sclerosis
Sturge-Weber syndrome
o Encephalo-trigeminal angiomatosis
o (1) capillary malformation of skin (port-wine birthmark) in trigeminal
distribution
o (2) retinal choroidal angioma
o (3) cerebral capillary-venous leptomeningeal angioma
o One of very few sponradic syndrome
o Pathogenesis
o Leptomeningeal (pia) angioma form multiple capillaries and venous
channels
o Common location : parietooccipital region
o 80% unilateral, ipsilateral to the facial angioma
o 20% bilateral
o Dystrophic laminar cortical calcification
o Presentation
o Nevus flammeus facial angioma visible at birth over the trigeminal
distribution (common V1-V2 distribution)
o 5% no nevus flaameus, lack of port-wine stain not rule out SWS
o And presence of port-wine stain birthmark not sufficient for diagnosis of SWS
o Seizure in the first year of life (75-90%) and often medially refactory
o Glaucoma
o Hemiparesis, migraine like headache
o Treatment : early lobectomy or hemispherectomy
o Imaging
o Sequelae of long-standing venous ischemia
o Progressive cerebral cortical subcortical atrophy
o CT findings
o NECT
o Dystrophic cortical/subcortical parenchymal calcifications
o Cortical/subcortical atrophy
o Enlarged ipsilateral choroid plexus
o CECT
o Enhancement of pial angioma
o Enalrged enhancing choroid plexus
NECT in an 8-year-old girl with SWS

- striking cortical atrophy
- extensive calcifications in the left cortex and subcortical WM
o MR findings
o T1WI : volume loss of affected cortex with enlargement of suarachnoid
space
o T2WI : linear hypointense of dystrophic cortical/subcortical calcification
with blooming on T2*
o FLAIR : serpentine hyperintense in the sulci ivy sign
o DWI : no restricted diffusion, unless acute ischemia
o T1WI + C : serpentine enhancement cover gyri extending to sulci,
enlarged medullary vein and ipsilateral choroid plexus
T2WI
Coronal T2* GRE
- Atrophy and thinned cortex with extensive

curvilinear hypointensity in the GM-WM
interface
- blooming of the extensive cortical-subcortical

calcifications
- Enlarged subarachnoid space with enlarged

traversing trabeculae and veins
Pial angioma
Medullary vein
Axial FLAIR scan in a 25-year-old woman with

seizures and SWS
T1 C+ FS scan
- the enhancing pial angioma fills the affected sulci
- left parietooccipital sulcal hyperintensity (ivy - linear enhancing foci, enlarged medullary veins,
sign).
provide collateral venous drainage into the
subependymal veins.
Tuberous sclerosis (TS)

o Non-malignant hamartomas and neoplastic lesion in multiple organs
o Triad (30% of cases)
o Facial lesion : adenomata sebaceum
o Seizure
o Mental retardation
o 50% autosomal dominant

o Four major features of the brain
o Cortical tubers
o Subependymal nodules
o Subependymal giant cell astrocytoma
o White matter lesions

o Imaging - abnormal in 98% of patients
o CT findings
o 1) Cortical tubers
o Hypo to isodense cortical/subcortical mass within broadened and expanded gyri
o Gyriform cortical calcification in 50% by 10 years
o 2) Subependymal nodules
o Found along caudathalamic groove
o Calcification increased with age
o No enhancement

o CT findings
o 3) White matter lesions
o Difficult to detect on CT
o 4) Subependymal giant cell astrocytoma

o
o
o
o
Heterogeneous density
Focal calcification
Common location : near Foramen of Monro
Moderate enhancement
NECT scan
NECT scan
CECT scan
- Calcified SENs
- Typical calcifications in subependymal - Enhancement adjacent to the

foramen of Monro, suspicious for
nodules.
- Wedge-shaped hypodensities
subependymal giant cell astrocytoma
characteristic of the WM lesions in
TSC

o MR findings
o More sensitive than CT
o 1) Cortical tubers
o In infant : Thickened hyperintense cortex (compared with underlying WM) on T1WI
and moderately hypointense on T2WI
o In older children : mixed SI on T2WI/FLAIR with isointense expanded gyrus at
periphery and strikingly hyperintense at deeper component
o 2) Subependymal nodules
o Small, nodular lesion form wall of lateral ventricles
o Hyperintense on T1WI, hypointense on T2WI and gradually become isointense with
WM with age
o Variable enhancement : strong enhancement in half, in contrast with CT

o MR findings
o 3) White matter lesions
o
o
o
o
Seen 100% of case

Streaky linear or wedge-shaped lesion extend radially from ventricle to cortex
In infant : hyperintense to WM on T1WI
In older children : hyperintense on T2/FLAIR
o 4) Subependymal giant cell astrocytoma

o
o
o
o
near Foramen of Monro

Mixed SI on both T1WI and T2WI
Moderately strong enhancement
Cause hydrocephalus
WM radial band
Axial T1WI in an 8-week-old male with TSC
- Multiple hyperintense noncalcified subependymal nodules

- Multiple hyperintense radial bands extending outward from the lateral
ventricles.
T1WI
T2WI
- Subependymal giant cell astrocytoma in the

right frontal horn.
- Linear and flame-shaped WM hyperintensities

under the cortical tubers.
- Expanded gyri characteristic of cortical tubers

T1WI
T1 C+
T2WI
- Classic appearance and location of - Mixed iso- and hypointense of SEGA

subependymal giant cell
typical cortical tubers with
astrocytomas near the foramen of characteristic WM lesions.
Monro.
- SEGAs enhancing intensely.
Epilepsy
Intracranial vascular malformation

o Epileptogenic vascular malformation
o 24-69% Arteriovenous malformation (AVM).
o 34-51% Cavernous malformation.
o Developmental venous anomalies and capillary telangiectasia are

clinically silent, not epileptogenic.
Arteriovenous malformation
o Congenital defect of vascular development.
o Tightly packed of thin wall vessels with direct arterial and venous
shunting
o Most AVMs are solitary lesion, < 2% multiple lesion --> Hereditary
hemorrhagic telangiectasia (Rendu-Osler-Weber disease)
o 85% supratentorial lesion, cerebral hemisphere
o 3 district components
o Feeding arteries
o Central nidus
o Draining veins
o Peak presentation 20-40 years of age
o Presentation
o Most common : headache with parenchymal hemorrhage
o Seizure and neurological deficits are initial symptoms in 25%
o Imaging
o CT findings
o NECT
o Numerous, slightly hyperdense serpentine vessel
o Calcification is common
o CECT
o Enhancement of all 3 components
NECT
- Serpentine hyperdensities
CECT
- Strong uniform enhancement wedgeshaped configuration
o MR findings
o Vary with vascular hemodynamics
o Tightly packed mass or honeycomb of flow voids on both T1 and T2
o Variable contrast enhancement, depend on flow rate
o Typically, draining vein is strongly and uniform enhancement
o Angiography
o Feeding arteries : enlarged and tortuous
o Nidus : tightly packed tangled of abnormal arteries and vein without
capillary bed
o Draining vein : opacified in mid to late arterial phase (early draining
vein)
T1WI
T2WI
- Extensive serpentine flow voids with multiple

venous varices
- Most of the large flow voids are enlarged

draining veins and venous varices
T2* GRE
T1 C+ FS
- No gross evidence of hemorrhage
- the serpentine flow voids enhance strongly,

uniformly.
Cavernous malformation
o Also known as cavernous angioma or cavernoma
o Benign malformative vascular hamartomas.
o Characteristic : Repeated intralesional hemorrhages, angiogenically
immature and blood filled locules caverns.
o Coexist with developmental venous anomalies (DVA)
o Presentation
o Half of all patients presents with seizures
o Headache
o Focal neurodeficit
o Imaging
o CT findings
o NECT
o Often normal
o May hyperdense with scattered intralesional calcification
o No mass effect
NECT
Punctate hyperdense lesion in the posterior
limb of the left internal capsule
o MRI findings
o Classic CCM
o Discrete popcorn ball lesion
o Mixed signal core surrounding with complete hemosiderin ring on T2WI

and bloom on T2*
o Enhancement is varies from none (common) to mild-moderate
T2WI
- Classic popcorn ball appearance with
locules of blood in different stages of
evolution
- Surrounded by hemosiderin rim
Infection/inflammation
o Rasmussens encephalitis
o Cysticercosis
Rasmussens encephalitis
o Chronic focal encephalitis
o Presentation
o Drug resistant epilepsy
o Progressive hemiparesis
o Mental impairment
o Treatment
o Immunomodulatory therapy, focal cortical resection, functional
hemispherectomy
Rasmussens encephalitis
o Imaging
o Initial imaging usually normal
o Developed Hyperintensity on T2/FLAIR in cortex and subcortical white
matter
o Unilateral progressive cortical (+/- basal ganglia) atrophy
o MRS : non-specific --> decreased NAA and increased Cho
Coronal FLAIR MRI of a young patient with

chronic right hemiconvulsion syndrome, 18
months after the initial event
- Diffuse atrophy of the left cerebral hemisphere
with T2 Hyperintensity within the white matter.
Epilepsy
Cortical and glial scar (Ulegyria)

o Cerebral cortex scarring due to perinatal ischemia
o Result from birth injury or meiningitis
o Usually affects full term infants
o Greater perfusion to apex of the gyri than to the cortex at the depth
of the sulci, resulting in shrunken cortex
o Deep portions of the gyri are more shrunken than the superficial
portions, leaveing pedunculated gyri on long stalk with mushroom
appearance
Common cause by age of patient

o 1 infant (< 18 months)
o 2. Patient 18 months 50 years of age
o 3. Mature patient (> 50 years)
Approach by age of patient

o 1 infant (< 18 months)
o 2. Patient 18 months 50 years of age
o 3. Mature patient (> 50 years)
Infant (<18 months)

o Primary considerations in neonates
o Infection.
o Perinatal cerebral vascular disease.
o Malformations of cortical development (MCD).
o Attention direct toward display of the lesion at the cortex

o Mesial temporal sclerosis is not a common in this age group -->
coronal oblique of hippocampus is not employed routinely.
Patient 18 months 50 years of age

o The highest yield for detection of structural pathology by MRI, including
hippocampal sclerosis.
o Administration of a contrast agent is not needed routinely unless there is
specific concern for tumor, vascular malformation, or infection.
o Exception for the patient with hemiatrophy, use of contrast enhancement
may reveal the Sturge-Weber malformation.
Mature patient (> 50 years)

o Primary consideration in patients older than age 50 years
o Stroke --> DWI is required to detect areas of ischemia
o neoplasm --> contrast agent should be administered routinely to help
detect neoplasms
o Hippocampal sclerosis is not common, so sequences for evaluation

of the hippocampus are not used routinely

Epilepsy

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TOPIC REVIEW

Advisor Assoc. Prof Sukulaya L. Radiologist

Seizure and Epilepsy

Seizure and Epilepsy

Imaging in epilepsy: a paediatric perspective, BrJR, 74 (2001).

Seizure and Epilepsy

Imaging in epilepsy: a paediatric perspective, BrJR, 74 (2001).

o Benign partial seizures with centrotemporal or occipital spikes

Imaging in epilepsy: a paediatric perspective, BrJR, 74 (2001).

Structural magnetic resonance imaging in epilepsy, Radiologa. 2012;54(1):9-20

o FLAIR sequences in the same planes should also be used to detect

Structural magnetic resonance imaging in epilepsy, Radiologa. 2012;54(1):9-20

Structural magnetic resonance imaging in epilepsy, Radiologa. 2012;54(1):9-20

Structural magnetic resonance imaging in epilepsy, Radiologa. 2012;54(1):9-20

Structural magnetic resonance imaging in epilepsy, Radiologa. 2012;54(1):9-20

T2WI and/or FLAIR Coronal perpendicular to hippocampus

Axial whole brain

Axial whole brain

Additional for specific lesion

Structural magnetic resonance imaging in epilepsy, Radiologa. 2012;54(1):9-20

Temporal lobe Limbic system

Temporal lobe Limbic system

Temporal lobe Limbic system

Temporal lobe Limbic system

Temporal lobe Limbic system

Temporal lobe Limbic system

Temporal lobe Limbic system

Limbic system - Hippocampus

Limbic system - Hippocampus

Osborns brain : imaging, pathology and anatomy, 1st edition

Limbic system - Hippocampus

Osborns brain : imaging, pathology and anatomy, 1st edition

Limbic system - Hippocampus

Osborns brain : imaging, pathology and anatomy, 1st edition

Temporal lobe Imaging anatomy

Temporal lobe Imaging anatomy

High resolution coronal T2WI

Temporal lobe Imaging anatomy

High resolution coronal T2WI

Osborns brain : imaging, pathology and anatomy, 1st edition

Mesial Temporal Sclerosis (MTS)

Osborns brain : imaging, pathology and anatomy, 1st edition

Mesial Temporal Sclerosis (MTS)

Coronal graphic of typical MTS

Osborns brain : imaging, pathology and anatomy, 1st edition

Mesial Temporal Sclerosis (MTS)

Mesial Temporal Sclerosis (MTS)

- T2/FLAIR : Hyperintensity with obscuration of hippocampal architecture on

A 37-year-old woman with temporal lobe epilepsy

Coronal true inversion recovery scan

Coronal thin-section T2WI

Shrunken left hippocampus

Hyperintensity of shrunken left hippocampus

Small ipsilateral fornix

mildly enlarged temporal horn is

Mesial Temporal Sclerosis (MTS)

Mesial Temporal Sclerosis (MTS)

Mesial Temporal Sclerosis (MTS)

Mesial Temporal Sclerosis (MTS)

Temporal Lobe Epilepsy: Quantitative MR Volumetry in Detection of Hippocampal Atrophy,

Mesial Temporal Sclerosis (MTS)

Mesial Temporal Sclerosis (MTS)

Mesial Temporal Sclerosis (MTS)

NO SIGN OF VOLUME LOSS !!!