Transcript Lecture 2 Powerpoint - McCausland Center | Brain Imaging

1
Introduction: Traumatic Brain Injury
Chris Rorden
– Deficits associated with focal injury
– Typical scanning modalities
2
Describing cortex location
Brodmann Areas (BAs, 1909)
Appearance of cortex under microscope
Not necessarily function
Arbitrary numbers are
hard to remember
3
Squirrels vs humans
squirrel brain
– Surface of human brain
is grooved.
– Surface of brain from
many animals is flat.
– If we completely flattened
a squirrel brain, it would
be the size of a stamp.
4
Cortical folding
Cortical folding increases surface area.
Ridges are called Gyri (singular = Gyrus)
– Greek gyros = circle, hence a coil of brain cortex
Valleys are called Sulci (singular = Sulcus).
– Latin = a groove.
Gyri
Sulci
5
Anatomy
Surface of human cortex and cerebellum is
very folded
– Flattened, each hemisphere 1100cm2
– Cerebellum is also 1100cm2
Crumpled shape hides size of cortex
– Compare Folded/Unfolded (from Marty Sereno)
Human
Chimpanzee
Monkey
6
Frontal Cortex (ch12)
Prefrontal cortex
– Dorsolateral) (DLPFC):
Executive control,
perseveration
– Oribitofrontal (OFC):
Inhibition, personality,
OCD
– Anterior Cingulate:
Abulia, Apathy
7
Hemispheres
Right Hemisphere Injury
Associated with Neglect
‘Dominant’ Left Hemisphere
Associated with Speech and
Language
8
Language Production
Broca’s Area (1861)
Difficulty in speech production
Loss of ability to repeat speech
Comprehension intact
Foot of 3rd frontal convolution
(BA 44)
Left hemisphere (1865)
– Except left handers
9
Language Comprehension
 Wernicke’s Area (1874)
 Normal production (speech sounds and
fluent nonsense)
 Sounds okay if you do not know the
patient’s language (e.g. Chinese
Wernicke’s aphasic would sound fine to
me)
 Unaware of deficit
 Impaired comprehension
 Left hemisphere
 Superior temporal gyrus
(BA 42, 22)
10
Wernicke’s prediction
Predicted two language centers:
– Broca’s Area: speech articulation.
– Wernicke’s Area: language comprehension.
Predicted 3rd Syndrome:
– Disconnection syndrome
– ‘Conduction aphasia’
– Damage to
arcuate fasciculus
11
Conduction aphasia
 Can comprehend speech
 Articulation is intact
 Difficulty in repeating speech
 Lesions in Temporal Parietal Junction that knock out
underlying white matter
 Patients with damage ONLY to the arcuate fasciculus
can still generate speech.
– Why? Other pathways
12
Wernicke-Lichtheim (1885) Schema
From auditory input (a) to motoric articulation
of speech (m)
Concepts
(Distributed)
Broca’s
Aphasia
Wernicke’s
Aphasia
Conduction
aphasia
13
Memory
Severe memory deficits seen with damage to Papez circuit.
Fornix (Squire’s
Patient)
Mammillary body
(Korsakoff Patients)
Hippocampal formation - HM
14
HM’s lesion
 Corkin et al. (1997)
 bilaterally symmetrical
–
–
–
–
medial temporal pole
most of the amygdaloid complex
most or all of the entorhinal cortex
anterior half of hippocampal formation (dentate gyrus, hippocampus, and
subicular complex)
15
HM – severe anterograde amnesia
Anterograde amnesia – since lesion
– Suggests encoding deficit
Retrograde amnesia – prior to lesion
anterograde
1/9/1953
Memory
retrograde
1945
1950
1955
16
Limbic system
Memory and
emotions
tightly
coupled.
Fear and
reward
17
Anatomy of t
Patients who spontaneously confabulate tend
to have orbitofrontal damage (aka damage to
the ventromedial PFC).
18
Frontal lobe injury
Personality
Executive function, organization, problem
solving
Set switching - Perseveration
19
The homonculus
Clear spatial mapping in gray
and white matter.
M1: movement
S1: sensation
20
Somatosensory Cortex
Woolsey and Wann (1976)
examined plasticity of
somatosensory cortex in mice.
Normally, cortical barrels
topographic map of space.
If whiskers removed, mapping of
remaining whiskers grows
21
Phantom Limbs
 MEG offers evidence of reorganization.
–
–
–
–
Patient lost one arm
When face is brushed, he experiences his old arm is touched.
Consistent spatial mapping of face to lost limb.
MEG reveals that arm and face encroach hand area
 Figure below: arm hand and face regions in normal locations contralateral
to intact arm, but arm and face representation have grown together
contralateral to lost limb.
– For review Ramachandran and Hirstein (2000), Brain, 121, 1603-1630
Arm
Hand
Face
22
Is plasticity reversible?
 Sirigu et al. (Nature Neuroscience, 4, 691-692).
– CD lost both hands in 1996
– Bilateral hand transplantation in 2000
– Both M1 and S1 show elbow activity had taken over hand
area before graft.
– After graft: hand area enlarges and elbow representation
shrinks.
23
Thought experiment
What brain injury leads to
visual field injury?
24
Mapping Lesions
With MRIcron it is easy to trace injured area.
We can create an overlay plot of damaged
region.
For example: here are the lesion maps for 36
people with visual field defects:
25
The problem with overlay plots
Overlay plots are misleading:
– Highlight areas involved with task (good)
– Highlight areas commonly damaged (bad)
Brain damage is not random: some brain areas
more vulnerable. Overlay plots highlight these
areas of common damage.
Solution: collect data from patients with similar
injury but without target deficit.
26
Value of control data
Solution: collect data from patients with similar
injury but without target deficit:
27
Statistical plots
We can use statistics to identify areas that
reliably predict deficit
E.G. Damage that results in visual field cuts
28
Acute brain imaging
Structural and perfusion imaging techniques
used at admission.
– Designed to be fast, does not require conscious
patient.
– In contrast, functional measures require
participation and typically have long duration
(future lectures).
29
CT versus MRI scans
 CT
– Clinically crucial:
 Detect acute hemorrhage
 Can be conducted when MRI contraindicated
– Limited research potential
 Exposes individual to radiation
• Difficult to collect control data
• Typically very thick slices, hard to normalize
 Little contrast between gray and white matter
 MRI
 Different contrasts
(T1,T2, DWI)
 No radiation, so we
can collect thin slices
if we have time.
30
Xrays and CT
 single contrast mechanism:
how well does tissue attenuate
rays.
 Air ~transparent, bone
~opaque, soft tissue
~translucent
 The only way to influence Xray
contrast is to change tissue.
E.G. injection of radio-opaque
Gd into bloodstream
Analogy: overhead projector ~ Xray
CT: reconstructed from series of Xrays
31
CT Terms
 Computerized Axial Tomography
(CAT/CT) measured Xray
attenuation.
– Hyperintensity: Bright spot
– Hypointensity: Dark spot
– For CT (but not MRI) you can say
‘density’ instead of ‘intensity’
– ‘W’/‘Window Width’ describes contrast
setting for display
– ‘C’/’L’/‘Window Center’/’WindowLevel’
describes brightness setting for display
32
Image Center/Width
How do we view an image
that has higher resolution
than our computer screen?
Panning changes the ‘image
center’.
Pan
– We will not see some of the
image.
Zooming changes the ‘image
width’.
– We may lose details.
Zoom
33
Intensity Center/Width (Brightness/Contrast)
 Adjust brightness ‘window center’
– E.G. range -64..124 makes muscles gray,
114..302 shows kidneys
– C/W 30/188 vs C/W 208/188
 Adjust contrast ‘window width’
– E.G. range -64..124 shows muscles,
-400..596 shows full range.
– C/W 30/188 vs C/W 98/996
 CT intensity is calibrated (kidneys
always ~208 Hounsfield units)
–
–
–
–
–
Air -1000
Water 0
White Matter 25
Gray Matter 40
Bone 1000
Pan
Zoom
34
CT Perfusion
 CT can be enhanced with a
contrast agent.
 For example, Gadolinium (Gd)
injected into the blood stream.
 Gd is radio-opaque.
 Can show areas of reduced,
delayed or slowed flow.
 Acute mismatch of perfusion
and injury shows tissue that
can be salvaged.
35
Major Cerebral Arteries
de Lucas E M et al. Radiographics
2008;28:1673-1687
Injury not
random:
common
patterns to
stroke and
TBI.
36
CT Signs of TBI
 Hematoma: pooled blood
 Contusion: swelling,
bruising.




EDH: epidural hematoma
DAI: diffuse axonal injury
SDH: subdural hematoma,
SAH/IVH: subarachnoid
and intraventricular
hemorrhage.
37
Magnetic Resonance Imaging (MRI)
 MRI uses strong magnetic field and
radio signals to acquire image.
 Analogy: Low energy state for
compass needle is North, but tap
briefly knocks out of alignment.
 Likewise, hydrogen atoms align to
field. Radio signal knocks them out of
alignment, they echo radio signals
while they return to alignment.
38
Conventional MRI scans
 T1 (anatomical): fast to acquire, excellent structural
detail (e.g. white and gray matter).
 T2 (pathological): slower to acquire, therefore usually
lower resolution than T1. Excellent for finding lesions.
T1
T2
Air
T1 CSF
Bone
T2
Air
GM
WM
GM
WM
Fat
CSF
edema
39
Lesion mapping: T1 vs T2



T1 scans offer good spatial resolution.
T2 scans better for identifying extent of injury, but
poor spatial resolution.
Solutions:
1. Acquire chronic T1 (>8 weeks)
2. Acquire both T1 and T2, use T2 to guide mapping on T1.
3. Acquire T2, map on normalized iconic brain (requires
expert lesion mapper).
4. Aquire high resolution T2 image, use for both mapping
and normalization (e.g. 1x1x1mm T2 ~9min). Requires
latest generation MRI.

Note: Many clinicians like FLAIR as it attenuates
CSF. Lesion signal similar to T2. Normalization
tricky (thick slices, no standard template).
T1
T2
FLAIR
40
Imaging acute stroke
 T1/T2 MRI and x-rays can not visualize
hyperacute ischemic strokes.
– Acute: Subtle low signal on T1, often difficult to
see, and high signal (hyperintense) on spin
density and/or T2-weighted and proton densityweighted images starting 8 h after onset. Mass
effect maximal at 24 h, sometimes starting 2 h
after onset.
– Subacute (1 wk or older): Low signal on T1, high
signal on T2-weighted images. Follows vascular
distribution. Revascularization and blood-brain
barrier breakdown may cause enhancement with
contrast agents.
– Old (several weeks to years): Low signal on T1,
high signal on T2. Mass effect disappears after 1
mo. Loss of tissue with large infarcts.
Parenchymal enhancement fades after several
months.
www.strokecenter.org/education/ct-mri_criteria/
acute
+3days
CT
T2
www.med.harvard.edu/AANLIB/
41
Imaging Hyperacute Stroke
 T1/T2 scans do not show acute injury.
 Diffusion and Perfusion weighted scans show
acute injury:
– Diffusion images show permanent injury. Perhaps
good predictor of eventual recovery.
– Perfusion scans show functional injury. Best correlate
of acute behavior.
– Difference between DWI and PWI is tissue that might
survive.
 Diaschisis: regions connected to damaged areas show acute
hypoperfusion and dysfunction.
 Hypoperfused regions may have enough collateral blood
supply to survive but not function correctly (misery perfusion).
T2
DW
42
Perfusion imaging
 Allows us to measure perfusion
– Static images can detect stenosis and
aneurysms (MRA)
– Dynamic images can measure perfusion (PWI)
 Measure latency – acute latency appears to be strong
predictor of functional deficits.
 Measure volume
– Perfusion imaging uses either Gadolinium or
blood as contrast agent.
 Gd offers strong signal. However, only a few boluses
can be used and requires medical team in case of
(very rare) anaphylaxis.
 Arterial Spin Labelling can be conducted continuously
(CASL). Good CASL requires good hardware.
43
MRI versus CT
MRI disadvantages:
– Expensive
– Slow to acquire
– Poor bone contrast
MRI advantages:
– No ionizing radiation
– Many contrast
modalities
– Some acute
modalities
44
T2 vs SWI for micro-hemorrhage
Susceptibility weighted imaging shows venous
blood useful for microbleeds, DAI
45
Diffuse Axonal Imaging
SWI and GRE images of individual with DAI