Neuroimaging in Epilepsy Flashcards
MRI Epilepsy Protocol includes
multiplanar diffuse T2 weight FLAIR GRE Susceptibility weighted imagings
3D volumetric T1 weighted acquision and oblique corolonal plane FLAIR and T2 weighted images through the long axis of temporal lobes
Epilepsy Surgical Options
Lesionectomy Corticectomy Topectomy corpus callosotomy hemispherectomy
MRI features of Temporal Lobe Epilepsy
MTS
Incomplete hippocampal inversion (best on oblique coronal plane)
Best sequences to diagnosis MTS
Oblique coronal temporal high resolution T2 weighted
FLAIR
MRI Findings of MTS
PRIMARY FINDINGS
- Hippocampal atrophy
- Increased T2 signal
- Abnormal morphology or loss of internal architecture of hippocampus
SECONDARY FINDINGS:
- Dilatation of temporal horn of lateral ventricle
- Loss of gray-white matter
- Differentiation in the temporal lobe or decreased white matter in adjacent temporal lobe
- Atrophy of ipsilateral fornix and mammillary body
How much % of cases of MTS are bilateral?
10%
What sequence is best for performing volumetric analysis?
3D T1WI
Neuronal migrational disorders on MRI
High resolution 3D T1 weighted volumetric imaging
Provides superior gray white contrast
Able to see subtle cortical malformations
Types of heterotopias
focal
nodular
multifocal (as in TS)
Preferentially involving one hemisphere
Subcortical bad heterotopias (SBH)
Periventricular
Bilateral nodular collections of gray matter with smooth margins
*Gives appearance of double cortex
Pachygyria
Abnormal tissues in the right location
-Abnormal sulcation and gyration mantel
>8mm thick
Polymicrogyria
Two or four layered clortex
<5-7mm
*Commonly associated with HIE, prenatal CMV
focal cortical dysplasia
Three categories:
Type I
Type IIa
Type IIb
Type III
Type 1 FCD
Subtle blurring of GW junction
Normla cortical thickness
Moderately increased hyperintensities T2/Flair
Decreased signal intensities on T1WI
Type IIA
Cortical dysplasias are characterized by:
-blurring of GW junction on T1 or T2/FLAIR
(due to hypomyelination/dysmyelination)
Transmantle sign = increase WM signal changes on T2, WI, FLAIR towards the ventricles
–> Signals radial glial neuronal bands
–> This is what distinguishes FCD and low grade tumors
*More commonly seen in extratemporal, esp in frontal regions
Type III FCD
Dual pathology
Associated with hippocamp sclerosis, tumor, vascular malformation
Lissencephaly
Smooth brain, abnormal gyration
IF posterior > LIS1 gene
IF anterior > subcortical band heterotopias (XLIS/DCX))
Schizencephaly
transcortical cleft extends from ventricles +/- open or fused lip (with polymicrogyria)
Hemimegalencephaly
Unilateral hamartomatous excessive growth of all or part of one cerebral hemisphere at different places of embryonic development
MRI findings in hemimeg
Enlarged hemisphere Increased white matter volume cortical thickening Agyria/pachygyria/Polymicrogyria/or lissencephaly Blurring of GW junction Ipsilateral irregular shaped ventricle
Brain tumors and incidence with seizures
20-40% with primary brain tumors (adults) experience seizure prior to onset
Another 20-45% will have seizures during course of illness
Seizures more common in which tumors?
Slow growing tumors:
Meningiomas, gangliogliomas, DNETs, diffuse low grade tumors (Grade II astrocytomas, oligodendrogliomas, oligoastrocytomas)
Most common location for tumors:
temporal >parietal >frontal >occipital
Gangliogliomas
- Where?
- Path?
- MRI features
- Temporal
- Path: contain mature neural ganglion cells, small mature neoplastic neurons
- MRI: tumors may show cystic changes or calcifications
DNETS
Where?
- Usually cortical based, benign
Meningioma
*Most common extra-axial tumors of CNS
Nonglial neoplasms that originate from arachnoid cap cells of meninges
Meningioma
Radiologic features
Isointense on T1 and T2; homogenous enhancement with gad, extra-axial dural tail
CSF cleft sign
Ganglioglioma
Radiologic features
Cyst with enhancing mural nodule/solid
Calcifications in 50%
DNET
Radiologic features
Bubbly cystic appearanc with small cysts within tumor
Hyperintense on T2WI
Wedge shaped mass which expands the affected gyri and point toward the ventricle
Swollen gyrus
May be associated with cortical dysplasia
Pleiomorphic Xanthoastrocytoma (PXA)
Supratentorial cyst with enhancing mural nodule which abuts the peripheral meninges, peritumoral edema, mild meningeal enhancement
Oligodendroglioma
Hypointense on T1, hyperintense on T2, calcification seen as areas of blooming
50% enhance heterogeneously
Minimal peritumoral edema
Hypothalamic hamartoma
Non-enhancing non-neoplastic congenital gray matter heterotopia in the region of the tuber cinerum of the hypothalamus, which can be sessile or pedunculated
Subependymal Giant Cell Astrocytoma (SEGA)
Heterogeneous mass near the foramen of monroe, usually >1 cm;
hypo or isointense on T1 and hyperintense on T2
+marked enhancement
Other findings of TS: cortical tubers, Subependymal nodules, transmantle sign, nodular ill-defined cystic and band-like lesions seen in the white matter and radial bands
Glioblastoma Multiforme
Hypo or isointense on T1, hyperintense on T2, vasogenic edema, susceptibility artifact on T2 from infratumoral lesions due to hemorrhage or rarely calcification
“butterfly glioma” when bilateral and cross the corpus callosum
-/+ necrosis
Peripheral or irregular nodular enhancement
No DWI restriction but lower ADC than low grade tumors
Metastases
Hypointense on T1 (except melanomas can be hyperintense)
Hyperintense on T2 and FLAIR
Intense enhancement (ring enhancing, punctate or uniform)
Often multiple lesions at diagnosis
Vasogenic edema out of proportion to size of lesion, hemorrhage, and necrosis
Gangliocytomas and Ganglineurocytoma
Gangliocytomas = Mature neural ganglion cells Ganglioneurocytomas = small mature neoplastic neurons MRI = show cystic changes or calcifications
High flow vascular malformations
AVM
Low flow vascular malformation
cerebral cavernous malformations (CCM)
Developmental venous anomaly (DVA)
Mixed vascular malformation
Imaging of cavernous malformations
MRI: Popcorn appearance with hemorrages of different ages*, area of hyperintensity representing methemoglobin surrounded by a hypointense ring of hemosiderin on T2W MRI, GRE helpful
CT = bright due to blood pooling within cavernoma
Imaging of AVM
MRI > CT
Better to appreciate fast flow on T2WI
Can see enlarged draining veins
MRA to subtract acute hemorrhage components from AVM
CTA = demonstrates feeding arteries, nidus, and draining veins
*Digital subtraction Angiography for delineating location of vessels
MEG Mechanism
MEG sensors are sensitive to magnetic fields that are orthogonal to head surface
-Electrical fields that are parallel to the scalp surfaces (specifically generated from sulcal banks)
vs EEG with is sensitive to radially oriented electrical fields at crests of gyri.
MEG Uses
Identifying spontaneous epileptic activity
Localize functional corticies using evoked responses to simple stimuli
- Use language tasks: word listening task or reading task
-Patient performs simple motor task
Objective of magnetic source modeling
Accounts for topography of the magnetic fields measured at a given point in time in the MEG sensors
Situations where MEG is helpful
Localizing epileptic pathology in refractory epilepsy or surgical work up
Especially in normal MR imaging, large or cystic lesions, or multifocal lesions or rapidly propagated spikes
Limitations of MEG
Localizes “irritative zones” not seizure onset zones
20% of patients , no spikes observed in recording
Not helpful for looking at networks
Not validated for mapping for language networks in anterior temporal or frontal neocortices to guid surgical boundaries.
MRI diffuse abnormalities during ICTAL phase of seizure
Primarily found on gray matter
Immediately –> increased electrical activity, leading to cellular metabolism and subsquent hyperperfusion
No apparent change in microarchitecture.
Then as seizure progressied –> vasogenic edema (ADC peak changes) then cytotoxic edema (decrease ADC)
