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Epilepsy Board Study > Neuroimaging in Epilepsy > Flashcards

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
Q

DNETS

Where?

A
  1. Usually cortical based, benign
26
Q

Meningioma

A

*Most common extra-axial tumors of CNS

Nonglial neoplasms that originate from arachnoid cap cells of meninges

27
Q

Meningioma

Radiologic features

A

Isointense on T1 and T2; homogenous enhancement with gad, extra-axial dural tail
CSF cleft sign

28
Q

Ganglioglioma

Radiologic features

A

Cyst with enhancing mural nodule/solid

Calcifications in 50%

29
Q

DNET

Radiologic features

A

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
Q

Pleiomorphic Xanthoastrocytoma (PXA)

A

Supratentorial cyst with enhancing mural nodule which abuts the peripheral meninges, peritumoral edema, mild meningeal enhancement

31
Q

Oligodendroglioma

A

Hypointense on T1, hyperintense on T2, calcification seen as areas of blooming
50% enhance heterogeneously
Minimal peritumoral edema

32
Q

Hypothalamic hamartoma

A

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
Q

Subependymal Giant Cell Astrocytoma (SEGA)

A

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
Q

Glioblastoma Multiforme

A

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
Q

Metastases

A

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
Q

Gangliocytomas and Ganglineurocytoma

A 
Gangliocytomas = Mature neural ganglion cells 
Ganglioneurocytomas = small mature neoplastic neurons
MRI = show cystic changes or calcifications
37
Q

High flow vascular malformations

A

AVM

38
Q

Low flow vascular malformation

A

cerebral cavernous malformations (CCM)
Developmental venous anomaly (DVA)
Mixed vascular malformation

39
Q

Imaging of cavernous malformations

A

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
Q

Imaging of AVM

A

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
Q

MEG Mechanism

A

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
Q

MEG Uses

A

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
Q

Objective of magnetic source modeling

A

Accounts for topography of the magnetic fields measured at a given point in time in the MEG sensors

44
Q

Situations where MEG is helpful

A

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
Q

Limitations of MEG

A

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
Q

MRI diffuse abnormalities during ICTAL phase of seizure

A

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)

Epilepsy Board Study (8 decks)

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