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Introduction: Traumatic Brain Injury
Chris Rorden– Deficits associated with focal injury– Typical scanning modalities
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Describing cortex location
Brodmann Areas (BAs, 1909)Appearance of cortex under microscopeNot necessarily function
Arbitrary numbers are hard to remember
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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.
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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
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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)
HumanChimpanzeeMonkey
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Frontal Cortex (ch12)
Prefrontal cortex– Dorsolateral) (DLPFC):
Executive control, perseveration
– Oribitofrontal (OFC): Inhibition, personality, OCD
– Anterior Cingulate: Abulia, Apathy
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Hemispheres
Right Hemisphere Injury Associated with Neglect
‘Dominant’ Left Hemisphere Associated with Speech and Language
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Language Production
Broca’s Area (1861)Difficulty in speech productionLoss of ability to repeat speechComprehension intactFoot of 3rd frontal convolution
(BA 44)Left hemisphere (1865)
– Except left handers
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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 deficitImpaired comprehensionLeft hemisphereSuperior temporal gyrus
(BA 42, 22)
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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
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Conduction aphasia
Can comprehend speechArticulation is intactDifficulty in repeating speechLesions in Temporal Parietal Junction that knock out
underlying white matterPatients with damage ONLY to the arcuate fasciculus
can still generate speech.– Why? Other pathways
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Wernicke-Lichtheim (1885) Schema
From auditory input (a) to motoric articulation of speech (m)
Broca’s Aphasia Wernicke’s
Aphasia
Concepts(Distributed)
Conduction aphasia
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Memory
Fornix (Squire’s Patient)
Mammillary body
(Korsakoff Patients)
Severe memory deficits seen with damage to Papez circuit.
Hippocampal formation - HM
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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)
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HM – severe anterograde amnesia
Anterograde amnesia – since lesion– Suggests encoding deficit
Retrograde amnesia – prior to lesion
1945 1950 1955
1/9/
1953
Mem
ory
anterograderetrograde
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Limbic system
Memory and emotions tightly coupled.
Fear and reward
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Anatomy of t
Patients who spontaneously confabulate tend to have orbitofrontal damage (aka damage to the ventromedial PFC).
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Frontal lobe injury
Personality Executive function, organization, problem
solvingSet switching - Perseveration
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The homonculus
Clear spatial mapping in gray and white matter.
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M1: movement
S1: sensation
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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
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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
ArmHandFace
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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.
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Thought experiment
What brain injury leads to visual field injury?
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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:
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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.
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Value of control data
Solution: collect data from patients with similar injury but without target deficit:
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Statistical plots
We can use statistics to identify areas that reliably predict deficit
E.G. Damage that results in visual field cuts
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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).
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CT versus MRI scans
CT– Clinically crucial:
Detect acute hemorrhageCan be conducted when MRI contraindicated
– Limited research potentialExposes individual to radiation
• Difficult to collect control data• Typically very thick slices, hard to normalize
Little contrast between gray and white matter MRIDifferent contrasts
(T1,T2, DWI)No radiation, so we
can collect thin slices if we have time.
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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
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Analogy: overhead projector ~ Xray
CT: reconstructed from series of Xrays
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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
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Image Center/Width
How do we view an image that has higher resolution than our computer screen?
Panning changes the ‘image center’.– We will not see some of the
image.Zooming changes the ‘image
width’.– We may lose details.
Pan
Zoom
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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
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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.
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Major Cerebral Arteries
Injury not random: common patterns to stroke and TBI.
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CT Signs of TBI
Hematoma: pooled bloodContusion: swelling,
bruising.
EDH: epidural hematomaDAI: diffuse axonal injurySDH: subdural hematoma,SAH/IVH: subarachnoid
and intraventricular hemorrhage.
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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.
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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
T2
T1 CSF
Bone
Air
Air
CSFWM GM
GM WM Fat
edema
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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
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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 density-weighted 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/www.med.harvard.edu/AANLIB/
T2
CT
acute +3days
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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
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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.
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MRI versus CT
MRI disadvantages:– Expensive– Slow to acquire– Poor bone contrast
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MRI advantages:– No ionizing radiation– Many contrast
modalities– Some acute
modalities
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T2 vs SWI for micro-hemorrhage
Susceptibility weighted imaging shows venous blood useful for microbleeds, DAI
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Diffuse Axonal Imaging
SWI and GRE images of individual with DAI
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