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17 Cards in this Set

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Mass effect
-disruption of capillaries or disturbance of vascular endothelial membranes during the original impact may lead to vasogenic cerebral edema
-as both hematoma and edema constitute mass effect, they raise intracranial pressure and may result in brain shift and cerebral hypoperfusion.
-brain herniations represent shift of the normal brain through or across regions to another site due to mass effect.
mass effect: damage to the brain due to the bulk of a tumor, the blockage of fluid, or excess accumulation of fluid w/in the skull
Cranial cavity
-the cranial cavity is partitioned by tentorium cerebelli and falx cerebri.
-when a part of the brain is compressed by an extrinsic lesion, such as a subdural hematoma, or is expanded b/c of a contusion or other intrinsic pathology, it is displaced (herniates) from one cranial compartment to another.
3 major herniations occur, either alone or in combo: what is the important one
Subfalcial herniation is displacement of the cingulate gyrus from one hemisphere to the other, under the falx cerebri.
Diaschisis
hypoperfusion and herniation lead to further brain damage in the form of pressure necrosis and infarction, often remote from the site of primary injury
-secondary lesions, unlike primary ones, are potentially avoidable if they are caught quickly and amenable to treatment, such as surgical evacuation of hematoma and edema therapy.
Anterior Cranial Fossa
-frontal lobes sit in the anterior fossa.
-anterior lateral aspects of the frontal bone swing around each of the frontal lobes, encapsulating them
-arising medially in the anterior cranial fossa is the crista galli, a bony protuberance of the ethmoid bone.
-it partially seperates the anterior ventral aspect of both frontal lobes and provides an anchor for the falx cerebri.
Middle Cranial Fossa
-bounds the temporal lobes
-formed by the temporal bone laterally and the greater wing of the sphenoid bone anteriorly and medially.
-sphenoid wing and ethmoid bone are quite irregular, jagged, and rough in some locations
Skull-Brain Interface
-w/ cerebral trauma, it is quite common for contusions to occur in cerebral regions adjacent to these skull regions where there is the greatest brain-bone interface
-MOST COMMON NEUROPATHOLOGICAL CONSEQUENCE: damage to the hippocampus and other medial temporal lobe limbic structures, resulting in post-traumatic memory disorder and emotional behavior changes.
-superficial bruising of gyral crests are frequently found in frontal and temporal regions regardless of the site or direction of initial impact
Primary Impact Damage: CHI typically gives rise to contusions and lacerations on or w/in the surface of the brain:
LACERATIONS
-lesions that break the pia mater
-usually found on the superficial crests of the gyri of the cerebral hemispheres, but they may penetrate the whole thickness of the cortex and extend into the subcortical white matter (OHI?).
-lacerations are hemorrhagic lesions which may lead to edema and necrosis w/in the brain
-usually heal and leave a yellow brown atrophic scars that are easily recognized on autopsy.
CONTUSIONS
Potential sites for cerebral contusion following CHI include:
-site of impact (coup)
-sites diametrically opposite site of impact (contrecoup)(equally damaging)
-frontal and temporal lobe crests
-surface lesions of the upper borders of the hemispheres
Diffuse axonal injury
-when the brain moves about violently inside the skull, the chances are very high that the axons will be stretched and torn. This is called diffuse axonal injury
-this is why shaken baby syndrome is such a serious form of child abuse.
-young childrens brains are very gelatinous and this kind of tearing can produce devastating injuries.
Causes of primary brain damage
-acceleration dependent factors
-non-acceleration dependent factors
-majority of CHIs involve acceleration dependent mechanisms
Types of primary damage assoc. w/ CHI
-acceleration/deceleration (mvmt of brain in skull)
-linear velocity damage-brain moves along linear path, causing damage at the site of impact and typically to anterior and inferior temporal and frontal lobes-often caused by blows to the back of the head
-angular acceleration injuries-brain rotates at an angle causing abrasions,lacerations, and twisting/shearing forces resulting in diffuse axonal injury, hemmorhage, and cranial nerve trauma-brain stem involved as the result of bony prominences in the skull and assoc. w/ frontolimbic injury *more worrisome
Acceleration Dependent Factors: Translational Trauma:
Causes
-pure translational trauma is exemplified by a sharply dealt blow to the occiput of a stationary but movable head.
-the head will rapidly accelerate forward
-because of inertia, the brain will lag behind until it is pushed forward by the advancing skull
-this lagging results in differential mvmts of the brain and the skull
-the delicate cortex is rubbed against rough surfaces of the dura-lined skull base.
-a not so pure example is when the accelerating head hits some unyielding surface, like a windshield.
-the skull decelerates to a sudden halt, but the brain continues to plunge forward at its accustomed velocity until it too is stopped by the frontal skull
-this site of initial brain impact w/ the skull, termed impact pole, causes the coup lesion
-the exact sequence of events reverses direction, and the brain lags behind the skull moving in the opposite direction
-the resulting injury at the antipole, at the site directly opposite the impact pole, is called the contrecoup lesion
-the deceleration process, in both directions, often takes several oscillations before the brain achieves zero velocity
Acceleration Dependent Factors: Translational Trauma:
Results
-the repeated slamming of the brain at the impact pole and antipole results in contusive coup and contrecoup lesions
-the brain also pulls away from the skull at the antipole causing greater tissue displacement and greater contrecoup injury
-moreover, the skull-brain interface will undergo several pendular swings, as the head rotates around it's vertical axis
-the cortex rubs repeatedly against the sharp dural edges of the falx, the sphenoid ridge, and the jagged floor of the anterior cranial fossa
-as a result, severe lacerations are often seen on the orbital frontal cortices and the tips of the frontal and temporal lobes
-w/ translational trauma the force applied to the skull is distributed over an appreciable area of the brain
Non-acceleration
a moving object hits the head (aka- impression trauma) and damage is localized and includes:
-impression trauma- meninges and cortex at site of impact are damaged as skull is deformed by a rapid blow. Negative pressure created by the rebound of skull may contribute to damage
-ellipsodial deformation-a slow-moving object w/ a lg. surface area deforms the skull from oval to circular shape-brain tissue moves outward from center resulting in stretching and tearing of central structures such as the basal ganglia e.g. tumor
Types of primary damage assoc. w/ penetrating head injury include:
-low-velocity- concentrated force causes fracture of the skull w/ debris enetring the brain - destruction of tissue at the site of impact is often substantial
-high-velocity- a projectile enters the brain- causes destruction of tissue around the projectile path
-main areas of damage from primary involvement are surface contusion, anterior and inferior frontal and temporal damage, bilateral temporal damage, frontolimbic damage, brain stem damage, basal ganglia damage
Types of secondary damage assoc. w/ penetrating head injury include:
hemmorhage
-extracerebral - bleeding into the meninges (epidural, subdural, subarachnoid)- epidural (arteries) may develop quickly and need immediate evacuation to avoid disability-subdural (veins) develop more slowly and are always associated w/ disability
-intracerebral- bleeding into the brain tissue - assoc. w/ diffuse axonal injury