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 ID: 717334
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Introduction: Traumatic Brain Injury
Chris Rorden
Deficits associated with focal injury
Typical scanning modalitiesSlide2
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Describing cortex location
Brodmann Areas (BAs, 1909)Appearance of cortex under microscopeNot necessarily functionArbitrary numbers are hard to rememberSlide3
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Squirrels vs humans
squirrel brainSurface 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.Slide4
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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 cortexValleys are called Sulci (singular = Sulcus).Latin = a groove.Gyri
SulciSlide5
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Anatomy
Surface of human cortex and cerebellum is very foldedFlattened, each hemisphere 1100cm2Cerebellum is also 1100cm2Crumpled shape hides size of cortexCompare Folded/Unfolded (from Marty Sereno)HumanChimpanzeeMonkeySlide6
Frontal Cortex (ch12)Prefrontal cortexDorsolateral) (DLPFC): Executive control, perseverationOribitofrontal (OFC): Inhibition, personality, OCDAnterior Cingulate: Abulia, Apathy
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HemispheresRight 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 handersSlide9
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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)Slide10
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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 fasciculusSlide11
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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 pathwaysSlide12
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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 Slide13
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Memory
Fornix (Squire
’
s Patient)
Mammillary body
(Korsakoff Patients)
Severe memory deficits seen with damage to
Papez
circuit.
Hippocampal formation - HMSlide14
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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)Slide15
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HM – severe anterograde amnesia
Anterograde amnesia – since lesionSuggests encoding deficitRetrograde amnesia – prior to lesion19451950
1955
1/9/1953
Memory
anterograde
retrogradeSlide16
Limbic systemMemory 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).Slide18
Frontal lobe injuryPersonality Executive function, organization, problem solvingSet switching - Perseveration
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The homonculusClear spatial mapping in gray and white matter.
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M1: movementS1: sensationSlide20
Somatosensory CortexWoolsey 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 armWhen 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 areaFigure 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
FaceSlide22
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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.Slide23
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Thought experiment
What brain injury leads to visual field injury?Slide24
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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:Slide25
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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.Slide26
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Value of control data
Solution: collect data from patients with similar injury but without target deficit:Slide27
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Statistical plots
We can use statistics to identify areas that reliably predict deficitE.G. Damage that results in visual field cutsSlide28
Acute brain imagingStructural 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
CTClinically crucial:Detect acute hemorrhageCan be conducted when MRI contraindicated Limited research potentialExposes individual to radiationDifficult to collect control dataTypically very thick slices, hard to normalizeLittle contrast between gray and white matter
MRI
Different contrasts (T1,T2, DWI)
No radiation, so we can collect thin slices if we have time.Slide30
Xrays and CTsingle contrast mechanism: how well does tissue attenuate rays.Air ~transparent, bone ~opaque, soft tissue ~translucentThe 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
XraysSlide31
CT TermsComputerized Axial Tomography (CAT/CT) measured Xray attenuation.Hyperintensity: Bright spotHypointensity: Dark spotFor 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
ZoomSlide33
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Intensity Center/Width (Brightness/Contrast)
Adjust brightness ‘window center’E.G. range -64..124 makes muscles gray, 114..302 shows kidneysC/W 30/188 vs C/W 208/188Adjust contrast ‘window width’E.G. range -64..124 shows muscles, -400..596 shows full range.C/W 30/188 vs C/W 98/996CT intensity is calibrated (kidneys always ~208 Hounsfield units)Air -1000Water 0White Matter 25Gray Matter 40Bone 1000
Pan
ZoomSlide34
CT PerfusionCT 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 ArteriesInjury not random: common patterns to stroke and TBI.
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de Lucas E M et al.
Radiographics
2008;28:1673-1687
©2008 by Radiological Society of North AmericaSlide36
CT Signs of TBIHematoma: 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
CSF
WM
GM
GM
WM
Fat
edemaSlide39
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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:Acquire chronic T1 (>8 weeks)Acquire both T1 and T2, use T2 to guide mapping on T1.Acquire T2, map on normalized iconic brain (requires expert lesion mapper).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
FLAIRSlide40
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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
+3daysSlide41
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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
DWSlide42
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Perfusion imaging
Allows us to measure perfusionStatic 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 volumePerfusion 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. Slide43
MRI versus CTMRI disadvantages:ExpensiveSlow to acquirePoor bone contrast
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MRI advantages:
No ionizing radiation
Many contrast modalities
Some acute modalitiesSlide44
T2 vs SWI for micro-hemorrhageSusceptibility weighted imaging shows venous blood useful for microbleeds, DAI
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Diffuse Axonal ImagingSWI and GRE images of individual with DAI
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