CNS Trauma Flashcards
Most Common/Important Event Post Severe TBI
Brain edema
Edema Progression
Begins as cytotoxic (intracellular) and progresses to vasogenic (EC, w/in 24 hours)
Cell Swelling
Astrocytes swell the most (cytotoxic), leading to breakdown of BBB (vasogenic)
Open Head Injury
Penetrating injury w/ depressed/displacing skull fracture, usually w/ laceration of dura
Treatments for Cytotoxic vs. Vasogenic
Osmotic agents to remove H2O vs. steroids
Closed Head Injury
No fracture or only linear fracture
Physical Mech/Anatomical Problems of Closed Head Injuries (2)
Higher mass of brain vs. skull so move/accelerate at different rates
Skull inside is rough and has ridges that can work like knives
4 Types of Lesions
Concussion (transient loss of consciousness)
Contusion (bruise - coup and countrecoup)
Laceration (tissue torn/disrupted)
Hemorrhage
Coup vs. Countrecoup Lesions
Side of blow, accelerating vs. opposite side, deccelerating
Plaque Jaune
Yellow plaques - when contusions heal w/ some pigment
Diffuse Axonal Injury (DAI)
Very severe brain injury from very violent episodes like car wrecks
3 Signs of DAI (1 gross, 2 histological)
Contusion on corpus callosum. Cortex might look fine
Spheroids on silver stain
Amyloid Precursor Prot (APP), like AD
Chronic Lesion DAI
Coma
Subdural Hematoma
From bridging veins on cortex initially, then granulation tissue encapsulates and its small veins can leak intermittently causing same effect as tumor. Between dura and arachnoid
4 People at Risk for Subdural Hematomas
Elderly
Alcoholics
Epileptics
Pts on Anticoagulants