Neuroimaging in Epilepsy Flashcards

1
Q

MRI Epilepsy Protocol includes

A
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

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2
Q

Epilepsy Surgical Options

A
Lesionectomy
Corticectomy
Topectomy
corpus callosotomy
hemispherectomy
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3
Q

MRI features of Temporal Lobe Epilepsy

A

MTS

Incomplete hippocampal inversion (best on oblique coronal plane)

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4
Q

Best sequences to diagnosis MTS

A

Oblique coronal temporal high resolution T2 weighted

FLAIR

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5
Q

MRI Findings of MTS

A

PRIMARY FINDINGS

  1. Hippocampal atrophy
  2. Increased T2 signal
  3. Abnormal morphology or loss of internal architecture of hippocampus

SECONDARY FINDINGS:

  1. Dilatation of temporal horn of lateral ventricle
  2. Loss of gray-white matter
  3. Differentiation in the temporal lobe or decreased white matter in adjacent temporal lobe
  4. Atrophy of ipsilateral fornix and mammillary body
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6
Q

How much % of cases of MTS are bilateral?

A

10%

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7
Q

What sequence is best for performing volumetric analysis?

A

3D T1WI

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8
Q

Neuronal migrational disorders on MRI

A

High resolution 3D T1 weighted volumetric imaging

Provides superior gray white contrast
Able to see subtle cortical malformations

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9
Q

Types of heterotopias

A

focal
nodular
multifocal (as in TS)
Preferentially involving one hemisphere

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10
Q

Subcortical bad heterotopias (SBH)

A

Periventricular
Bilateral nodular collections of gray matter with smooth margins
*Gives appearance of double cortex

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11
Q

Pachygyria

A

Abnormal tissues in the right location
-Abnormal sulcation and gyration mantel
>8mm thick

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12
Q

Polymicrogyria

A

Two or four layered clortex
<5-7mm
*Commonly associated with HIE, prenatal CMV

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13
Q

focal cortical dysplasia

Three categories:

A

Type I
Type IIa
Type IIb
Type III

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14
Q

Type 1 FCD

A

Subtle blurring of GW junction
Normla cortical thickness
Moderately increased hyperintensities T2/Flair
Decreased signal intensities on T1WI

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15
Q

Type IIA

A

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

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16
Q

Type III FCD

A

Dual pathology

Associated with hippocamp sclerosis, tumor, vascular malformation

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17
Q

Lissencephaly

A

Smooth brain, abnormal gyration

IF posterior > LIS1 gene
IF anterior > subcortical band heterotopias (XLIS/DCX))

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18
Q

Schizencephaly

A

transcortical cleft extends from ventricles +/- open or fused lip (with polymicrogyria)

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19
Q

Hemimegalencephaly

A

Unilateral hamartomatous excessive growth of all or part of one cerebral hemisphere at different places of embryonic development

20
Q

MRI findings in hemimeg

A
Enlarged hemisphere 
Increased white matter volume
cortical thickening
Agyria/pachygyria/Polymicrogyria/or lissencephaly
Blurring of GW junction 
Ipsilateral irregular shaped ventricle
21
Q

Brain tumors and incidence with seizures

A

20-40% with primary brain tumors (adults) experience seizure prior to onset
Another 20-45% will have seizures during course of illness

22
Q

Seizures more common in which tumors?

A

Slow growing tumors:
Meningiomas, gangliogliomas, DNETs, diffuse low grade tumors (Grade II astrocytomas, oligodendrogliomas, oligoastrocytomas)

23
Q

Most common location for tumors:

A

temporal >parietal >frontal >occipital

24
Q

Gangliogliomas

  1. Where?
  2. Path?
  3. MRI features
A
  1. Temporal
  2. Path: contain mature neural ganglion cells, small mature neoplastic neurons
  3. MRI: tumors may show cystic changes or calcifications
25
DNETS | Where?
1. Usually cortical based, benign
26
Meningioma
*Most common extra-axial tumors of CNS | Nonglial neoplasms that originate from arachnoid cap cells of meninges
27
Meningioma | Radiologic features
Isointense on T1 and T2; homogenous enhancement with gad, extra-axial dural tail CSF cleft sign
28
Ganglioglioma | Radiologic features
Cyst with enhancing mural nodule/solid | Calcifications in 50%
29
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
30
Pleiomorphic Xanthoastrocytoma (PXA)
Supratentorial cyst with enhancing mural nodule which abuts the peripheral meninges, peritumoral edema, mild meningeal enhancement
31
Oligodendroglioma
Hypointense on T1, hyperintense on T2, calcification seen as areas of blooming 50% enhance heterogeneously Minimal peritumoral edema
32
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
33
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
34
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
35
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
36
Gangliocytomas and Ganglineurocytoma
``` Gangliocytomas = Mature neural ganglion cells Ganglioneurocytomas = small mature neoplastic neurons MRI = show cystic changes or calcifications ```
37
High flow vascular malformations
AVM
38
Low flow vascular malformation
cerebral cavernous malformations (CCM) Developmental venous anomaly (DVA) Mixed vascular malformation
39
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
40
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
41
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.
42
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
43
Objective of magnetic source modeling
Accounts for topography of the magnetic fields measured at a given point in time in the MEG sensors
44
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
45
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.
46
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)