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C3 CLINICAL > Epilepsy: Structural Imaging and Novel Contrasts > Flashcards

Epilepsy: Structural Imaging and Novel Contrasts Flashcards

1
Q

What is the NICE guidelines on epilepsy (2012)?

A
  1. MRI should be the imaging investigation of choice in children, young people and adults with epilepsy
  2. Particularly onset before 2yr or in adulthood, focal onset seizures, pharmacoresistant epilepsy
  3. Should be performed soon (within 4 weeks)
  4. Not required for idiopathic generalised epilepsy
  5. CT if MRI not available/contraindicated, in children who would need anaesthetic/sedation for MRI and in acute situation (e.g. bleed)
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2
Q

When and why is imaging useful?

A
  1. New onset focal seizures
    - identification of cause e.g. tumour
  2. Refractor focal seizures
    - assessment for surgical treatment
    - what is nature of lesion?
    - what is extent of lesion?
    - what is relationship of lesion to eloquent cortex
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3
Q

What is the acquisition protocol (ILAE, Bonn)?

A
  1. 3D volumetric T1-weighted - grey/white matter contrast, cortical thickness, MCD
  2. T2-weighted (axial,coronal) - hippocampal architecture (long axis), cystic tissue components
  3. FLAIR (axial, coronal) - hippocampal sclerosis, FCD, tumours, inflammation, scars
  4. T2* gradient echo echo/ SWI (axial) - calcifies or vascular e.g. caverns, AVM
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4
Q

What is the imaging hardware/ scan interpretation?

A
  1. Increased field strength, better coils, gradients
    - better SNR, resolution, hippocampal subfields (7T)
    - distortions/artefacts, patient tolerance, expense
  2. Chalfont series of > 800 patients on 1.5T vs 3T
    - 37(5%) new diagnoses esp. HS, FCD, DNET
  3. Diagnostic yield in presurgical epilepsy MRI
    - 1.5T standard - non-expert (39%), expert (50%)
    - 1.5T epilepsy protocol - expert (91%)
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5
Q

What are example MRI findings?

A
  1. Hippocampal sclerosis
  2. Malformations of cortical development
    - focal cortical dysplasia
    - cortical neoplasms
  3. Meningioma
  4. Vascular malformations
  5. Infectious (worldwide)
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6
Q

What is Hippocampal Sclerosis?

A
  1. Most common cause of refractory TLE
    - neuronal fell loss/gliosis esp. CA1, CA3, dentate gyrus
  2. Visual analysis alone may fail to detect HS
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7
Q

What are the imaging features of Hippocampal Sclerosis?

A
  1. Hippocampal atrophy
  2. Disrupted internal architecture
  3. Decreased T1-weighted signal
  4. Increased T2-weighted signal
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8
Q

What is malformations of cortical development?

A
  1. Updated classification scheme (>200 categories)
  2. Neuronal/glial proliferation of apoptosis
  3. Neuronal migration
  4. Postmigrational development
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9
Q

What are examples of abnormal neuronal/glial proliferation or apoptosis?

A
  1. Microcephaly
  2. Megalencephaly
  3. Cortical dysgenesis with abnormal cell proliferation (e.g. FCD II, TS)
  4. Cortical dysgenesis with abnormal cell proliferation and neoplasia (e.g. DNET, ganglioglioma)
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10
Q

What is Hemimegalencephaly?

A
  1. Unilateral cortical enlargement
  2. Large, asymmetrical head
  3. Epilepsy +/- learning disability
  4. Large ventricle
  5. Abnormal sulcation
  6. Cortical thickening
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11
Q

What are examples of abnormal neuronal migration?

A
  1. Heterotopia
  2. Lissencephaly
  3. Subcortical heterotopia, sublobar dysgenesis
  4. Cobblestone malformation
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12
Q

What are examples of abnormal postmigrational development?

A
  1. Polymicrogyria, schizencephaly
  2. Cortical dysgenesis secondary to inborn errors of metabolism
  3. Focal cortical dysplasia (including FCD I, III)
  4. Postmigrational Microcephaly
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13
Q

What is polymicrogyria ?

A
  1. Excessive small gyri
    - focal or generalised
  2. Epilepsy, learning disability, speech/swallowing/respiratory
  3. Genetic
    - viral
    - nutritional deficits
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14
Q

What are focal cortical dysplasia ?

A
  1. Up to 42% of MRI-negative patients undergoing surgery have FCD
  2. Disrupted laminar architecture and columnar organisation and abnormal cells, including dua moronic neurons and balloons cells
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15
Q

What are imaging features of focal cortical dysplasia?

A
  1. Cortical thickening and blurring grey/white matter boundary (T1-weighted)
  2. Cortical/sub-cortical signal hyper intensity (T2-weighted)
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16
Q

What are the different types of focal cortical dysplasia?

A
  1. Prior classification system (Palmini 2004) updated 2011
  2. Type I (abnormal cortical layering)
    - type Ia - abnormal RADIAL cortical Lamination
    - type Ib - abnormal TANGENITAL cortical lamination
    - type Ic - abnormal RADIAL + TANGENITAL
  3. Type II (disrupted lamination + cytologic abnormalities)
    - type IIa - dysmorphic neurons
    - type IIb - dysmorphic neurons + balloon cells
  4. Type III (disrupted lamination + primary lesions)
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17
Q

Why is finding a lesion so important?

A
  1. Surgical target!
  2. Each type has varied MR findings
    - IIb associated with less wide spread abnormalities (both structural and functional)
    - more favourable seizure outcome after epilepsy surgery compared to types I and IIa
18
Q

What is the most common cortical neoplasms?

A
  1. Ganglioglioma

2. Low grade astrocytoma

19
Q

What are less common cortical neoplasms?

A
  1. Low-grade oligodendroglioma

2. DNET

20
Q

What is nearly exclusively seen in epilepsy?

A
  1. Ganglioglioma

2. DNET

21
Q

What is Meningioma?

A
  1. Commonest extra-axial tumour

2. 20-50% have epilepsy as presenting symptoms

22
Q

What is vascular abnormalities?

A
  1. Cavernoma - heterogenous core depending on age of blood products, outer rim T2 hypointense
  2. GRE (T2*) or SWI sequences useful for detection
23
Q

What is MRI negative epilepsy?

A
  1. Around 30% of patients with focal epilepsy have normal conventional MRI (“MRI negative”)
    - undetected hippocampal sclerosis/ FCD
    - implications on surgery/planning/surgical outcome
24
Q

What are the possible solutions for MRI negative Epilepsy?

A
  1. Quantitative analysis
  2. Post-processing/computational techniques
  3. Novel image contrasts
  4. Varies from centre to centre
25
Q

What is Quantitative assessment of HS?

A
  1. Hippocampal volumetric
    - manual
    - automated
  2. Hippocampal T2 relaxometry
    - manual
    - automated
  3. Quantitation improves sensitivity to detect HS
  4. 28% in “MR Negative”
26
Q

What is automated Hippocampal segmentation?

A
  1. Manual: time-consuming and subject to interrater/Intrarater variability
  2. Automated: reduce time commitment, reproducible
    - some techniques perform poorly in abnormal atrophic hippocampi
  3. Useful in identifying subtle or bilateral pathology
27
Q

What is Automated T2 mapping?

A
  1. Dual-echo spin-echo sequence (PD,T2) - full brain coverage with sufficient sensitivity
  2. Manual delineation is time consuming & samples part of hippocampus with CSF contamination
  3. Can take Hippocampal segmentation, register to PD/T2 , erode, remove voxels with high T2(CSF)
  4. Automated more reproducible than manual T2 relaxometry
28
Q

What are post-processing/computational methods?

A
  1. Voxel-based approach
  2. Surface-based approach
  3. Combinations using machine learning models
29
Q

What are voxel-based approaches to FCD?

A
  1. Investigate differences in brain anatomy statistically
  2. Spatially normalise you group template + segment
  3. Smooth + compare individual to controls on voxelwise basis
    - grey matter (from T1)
    - signal intensify (from FLAIR)
    - derivatives e.g. junction map
  4. Main limitations is poor specificity
30
Q

What is surface-based approaches to FCD?

A

Morphometric measures from geometric surface models - individual curvature and folding

  1. Extract cortical surface
    - Paul surface (CSF/dura + grey matter)
    - white surface (grey matter + white matter)
  2. Represent as surface model (triangular mesh)
  3. Morphometric measures
    - cortical thickness
    - cortical curvature
  4. Surfaces can be inflated (match folding) to enable comparisons between groups
31
Q

What are free surfer parakeets for surface-based approaches to FCD?

A
  1. Cortical thickness
  2. GM/WM contrast
  3. Local gyrification index
  4. Sulcal depth
  5. Mean curvature
32
Q

What is diffusion imaging?

A
  1. In CSF, water diffuses equally in all directions
  2. In white matter, water diffuses along length of nerves rather than perpendicular
  3. Diffusion imaging is an MRI sequence that quantified water diffusion in different directions
33
Q

What are parameters of diffusion imaging?

A

FA (fractional anisotropy)

  • quantifies degrees of directionality of diffusion
  • ranges from 0 (isotropic) to 1 (fully anisotropic)
  • often reduced in disease (e.g. hippocampal sclerosis)

MD (mean diffusivity)

  • quantified average rate of diffusion in all directions
  • often increased in disease
34
Q

What is magnetisation transfer imaging?

A
  1. Protons exist in two pools - free and bound
    - magnetisation pulse applied to exclusively bound pool (macromolecules)
    - energy transferred to free pool
    - contrast generated from magnetisation exchange
    - quantified as MTR (magnetisation transfer ratio)
    - reduced due to loss of macromolecules
35
Q

What are the results of MTR?

A
  1. 15/42 MRI-negative epilepsy
    - changes concord ant with electro clinical syndromes
    - minor structural disorganisation
36
Q

What is double inversion recovery?

A
  1. Two inversion pulses to bull signal from CSF (like FLAIR) and from normal white matter
  2. Useful to visualise cortical ribbon with minimisation of CSF/WM partial volume effects
37
Q

What are limitations of techniques?

A
  1. Limited sensitivity and different sequences perform differently
  2. Problem of lack of specificity so many false positives
  3. Never really introduced into clinical practice
  4. Future approaches
    - computational post-processing of multiple contrasts
    (E.g. machine learning)
38
Q

What is ASL?

A
  1. Non-invasive, ionisation free measure of tissue perfusion
  2. Magnetically labelled arterial blood eater protons as an endogenous tracer
39
Q

What do areas of low perfusion correspond to in ASL?

A

Areas of reduced glucose metabolism (on FDG-PET)

40
Q

What is NODDI?

A
  1. Neurotransmission orientation dispersion and density imaging
    - special type of diffusion-weighted scan and modelling, provides estimates of tissue microstructure
  2. May identify reduced intracellular volume fraction, marker of neurite density - FCD
41
Q

What is the principle of multimodal imaging?

A
  1. Co-register and display multiple imaging sources in a common space to understand the 3D relationship between different metabolites
  2. Useful for planning of the 20-30% of patients who require intracranial EEF
  3. Increasing move towards SEEG (12-29 depth)
    - practice targeting (entry,destination) increases grey matter sampling and reduced risk (arteries,veins)

C3 CLINICAL (27 decks)

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