Post on 21-Feb-2022
Brain Trauma
Majda M Thurnher
• The skull provides the brain with a protective thick, bony encasement
• yet its irregular interior presents opportunities for damage to the fragile tissues it has evolved to protect
Traumatic Brain Injury (TBI)
Glasgow Coma Scale
The Glasgow Coma Scale is based on a 15 point scale for estimating and categorizing the outcomes of brain injury on the basis of overall social capability or dependence on others.
Mild (13-15):
Moderate Disability (9-12):Loss of consciousness greater than 30 minutesPhysical or cognitive impairments which may resolve
Severe Disability (3-8):Coma: unconscious state.No meaningful response, no voluntary activities
Vegetative State (Less Than 3):Sleep wake cyclesArousal, but no interaction with environmentNo localized response to pain
Classification of TBI
• Mechanism: closed or penetrating
• Severity: mild, moderate, severe
• Pathology: primary or secondary
• Morphology: focal or diffuse
1. PRIMARY HEAD INJURYScalp injuriesSkull fracturesExtra-axial hemorrhagesIntra-axial injuries
2. SECONDARY HEAD INJURYIschemiaHypoxiaHypotensionCerebral edemaMeningitis / AbscessIncreased intracranial pressure
Classification of TBI Primary brain injury refers to the sudden and profound injury to the brain that is considered to be more or less complete at the time of impact.
Secondary brain injury refers to the changes that evolve over a period of time (from hours to days) after the primary brain injury.
It includes an entire cascade of cellular, chemical, tissue, or blood vessel changes in the brain that contribute to further destruction of brain tissue.
1. PRIMARY HEAD INJURY
Scalp injuries
Skull fractures
Extra-axial hemorrhages
Intra-axial injuries
Epidural hematoma Subdural hematoma
Extra-axial hemorrhages
Subarachnoid &intraventricular hemorrhage
Epidural Hematoma (EDH)
Blood collection in space between inner table of skull and outer layer of dura
• Laceration or tearing of meningeal arteries• 90% arterial • 10% venous
• YOUNG ADULTS, rare in elderly• M:F 4:1
Epidural Hematoma (EDH)
NECT• hyperdense• biconvex or lenticular-shaped• smooth• compresses underlying brain• midline shift• does not cross sutures
(dura is attached to the calvarium tightly along the sutures)
Epidural Hematoma (EDH)
• Internal hypodense component
• Active bleeding with unretractedcloth
SWIRL SIGN
• Adjacent to venous sinus• Fracture through sinus• Slow accumulation of blood • Can cross falx and tentorium
Venous Epidural Hematoma Anterior temporal venous EDH
Sphenoparietalal sinus
Vertex Venous EDH
Superior sagittal sinus
Venous Vertex EDH
Delayed Epidural Hematoma
At Presentation 24 Hours Later
• overall mortality 5%, bilateral EDH 15-20%• 10-25% will show enlargement within 1-36 h(“lucid interval” before it becomes large enough to cause unconsciousness)
• majority require surgical evacuation
• the bleeding stops when intracranial pressure exceeds arterial pressure
Therapy and prognosis of EDH
Blood collection in subdural space
Subdural Hematoma (SDH) • Tearing of bridging cortical veins• most common in ELDERLY
• no gender predilection
ng of bridging cortical veinsSubdural Hematoma (SDH)
• Supratentorial convexity• Posterior fossa, along the falx • Adjacent to the tentorium
Subdural Hematoma (SDH)
Acute SDH > 1 week
Subacute SDH 1-3 weeks
Chronic SDH > 3 weeks
Subdural Hematoma (SDH)
• sickle-shaped, crescentic • 60% hyperdense• 40% mixed • smooth defined borders• may cross sutures• compression of the ventricle• midline shift• may have SWIRL SIGN
Acute Subdural Hematoma (a (aSDHH)
“Subdural window setting”
Window 150-300 HU
Center/level 50-100 HU
Isodense or hypodense aSDH
• Anemia (low Hemoglobin)• Hematoma without clot• Tears in pia/arachnoid membrane result in CSF
leakage into SDH = dilution • Coagulopathy
Subdural Hematoma (SDH)
CAVEAT!
NECT• mixed density (recurrent hemorrhage) • gray-white junction displaced medially (“thick cortex”)• „dots“ of CSF = displaced cortical vessels
CECT• enhancement of the dura and membranes
Subacutee Subdural Hematoma (a (sSDHH)
NECT• sickle-shaped, crescentic • MULTISEPTATED• variable density (mostly CSF density)• calcifications
CECT• enhancement of the dura and membranes
Chronic Subdural Hematoma (a (cSDHH)
Homogenous/ laminar
Chronic Subdural Hematoma (a (cSDHH)
Separated (hematocrit level)
Trabecular (internal septae, calcifications)
What can happen to cSDH?
Resolve spontaneously
Continue to grow
Re-hemorrhageSerum protein exsudation
Chronic Subdural Hematoma (a (cSDHH)
CSF collection in subdural space
Subdural Hygroma
• traumatic tears in the arachnoid membrane
• usually 4-30 days (mean 9 days) after trauma
• NO membranes• children: hematohygroma
Subdural Hygroma
• mortality 35-90%• hematoma thickness, midline shift > 2 cm
requires surgical evacuation
Therapy and prognosis SDH
Blood within subarachnoid spaces
Subarachnoid Hemorrhage (SAH)
• Tearing of vessels in subarachnoid space• young age, chronic alcohol abuse• M:F 2:1
• Midline SAH is associated with DAI!
• Cause vasospasm much less frequently
Traumatic Subarachnoid raumatic SubarachnoidHemorrhage (SAH)
NECT• high density in subarachnoid spaces• blood in interpeduncular cistern!• adjacent to contusions• convexity > basal
• focal or diffuse
Subarachnoid Hemorrhage (SAB)
FLAIR is the most sensitive
MRI technique in detection of SAH
Wu Z et al. Evaluation of tSAH using SWI. AJNR 2010
• smooth-looking veins• rough boundaryinhomogeneous SAH
Susceptibilityty-y-weighted MR imaging Pseudodo-o-SAH • Seen in diffuse brain edema• Due to pial vessel engorgement and/or
contraction of the subarachnoid space
Hasan TF et al. Journal of Stroke and Cerebrovascular Diseases 2018
Pseudodo-o-SAH • Seen with bilateral SDH
• Rotationally induced tearing of subependymal veins on the ventral surface of the corpus callosum and along the fornix and septum pellucidum
• spread from parenchymal bleed
• retrograde influx of SAH
Intraventricularar Hemorrhage (IVH)
1. PRIMARY HEAD INJURY
Scalp injuries
Skull fractures
Extra-axial hemorrhages
Intra-axial injuries
Brain surface injury involving gray matter and contiguous white matter
Cerebral Contusion
• Bruises of the brain parenchyma
• Stationary head struck by object• Moving head (traffic, falls)
• Can increase in size (first 48 h)
• M:F 3:1• children : adults 2:1
Cerebral Contusion
Location• anterior inferior frontal lobe• anterior inferior temporal lobe• parietal/occipital lobes• posterior fossa
Cerebral Contusion
COUP (blow)
• direct injury to brain beneath impact site• brain hitting the interior of the skull
CONTRECOUP (against the blow)
• injury opposite impact site• due to process called cavitation
Cerebral Contusion
Hemorrhagic Contusions
Tonsillar hemorrhagic contusions after being hit with a baseball bat in the back of the
head
Cerebral Hematoma
• Collection of confluent, homogeneous blood in the brain parenchyma
• Deeper part of the brain
• Less edema
Brain tissue and blood Blood
Contusion Hematoma
“Release Hematoma”
• Shearing injuries resulting from abnormal rotation or deceleration of adjacent tissues that differ in density or rigidity
• any age, most common young adults• M:F 2:1
When the head moves, the brain also moves. The different layers of the brain move at different times
because each layer has a different density.
Diffuse axonal injury (DAI)
• axons STRETCHED (rarely disconnected)
• metabolic alterations• cellular swelling• cytotoxic edema • apoptosis
Diffuse axonal injury (DAI)
• gray-white matter junction• frontal and temporal• corpus callosum (splenium)• brainstem (dorsolateral midbrain)
• deep GM, internal capsule, fornix, corona radiata• cerebellar peduncle
Diffuse axonal injury (DAI)
Adams and Gennarelli staging
Stage 1 GM/WM junction (mild TBI)
Stage 2 lobar WM, corpus callosum (moderate TBI)
Stage 3 midbrain, pons (severe TBI)
Diffuse axonal injury (DAI)
NECT50-80 % NORMALsmall hypodense foci
small hyperdense foci
10-20% focal mass lesion
MRImultiple,
small focal lesions
oval, elliptic
punctate -15 mm
Diffuse axonal injury (DAI)
Hemorrhagic Shearing Injuries
Hergan K et al. Diffusion-weighted MRI in diffuse axonal injury of the brain. Eur Radiol 2002
Diffusionon-n-weighted MR imaging
a) Cytotoxic edemaa)b)
Cytotoxic edemaVasogenic edemab)
c)Vasogenic edemaCentral hemorrhage with cytotoxic edema
GRE
T2
DWI
Courtesy T Huisman
Splenial shear
C/o J. Ocampo, Argentina
Susceptibilityty-y-weighted MR imaging (SWI)
GRE SWI
Courtesy Mauricio Castillo
• A type of shearing injuries– Shearing of the perforating (lenticulostriate) arteries
supplying the basal ganglia
• Generally bilateral, asymmetrical• May have fluid/blood levels• Poor prognosis
Intermediary injuries
• Rare compared to DAI• High impact MVAs• 12% of fatal injuries• Immediate unconsciousness• Subcortical, deep WM, BG• Frontal, temporal lobes
Courtesy of Anne Osborn
Diffuse vascular injury (DVI)
Courtesy Anne Osborn28 years-old male patient with head trauma, GCS=5
• DVI and DAI are not separate entities but have a closerelationship and that there may be a spectrum or at least a continuum between DAI and DVI
Diffuse vascular injury (DVI)
• Hemorrhages are distrubutedalong the perimedullary veinswhich drain into septal veins
Missile and Penetrating Injuries
Cranial trauma from high-velocity projectile (gunshot, sharp objects)
• Pressure wave in front of missile crushes / stretches tissue, creates temporary cavitation• Traumatic pseudoaneurysm• Vascular transection
ENTRY SITE • soft tissue injury• bone fragments• bullet
HEMORRHAGIC TRACT through brain
HEMORRHAGES (SDH, EDH, SAH)
EXIT SITE
Missile and Penetrating Injuries
Arrow
GSW
Pencil Pen
KnifeCrowbar
Arrow Picket fence
Pneumatic drill bit
Courtesy M Castillo