Brain Injury Flashcards
CNS vs PNS
CNS
- UMN: cortical, brainstem
- other: basal ganglia, cerebellum, other
Brain Injury causes
-falls 36%
-MVA 26%
-objects 24%
-assault 14%
sports-related TBI is 2nd only to MVA
pediatric TBI
- most common cause of physical disability can cognitive impairment in young people
- MOI: MVA or isolated pediatric head injury
Neuroanatomy
- layer of protection: meningeal layers
- anterior, middle, and posterior fossae and contents
tenorium cerebelli
differentiates supra (cortex) and infra (cerebellum) tentorium regions
tentorial notch
where a herniation can occur
types of pathogenesis
axonal shearing cerebral contusions and hemorrhage subdural hematoma epidural hematoma concussion
Primary vs secondary injury
primary-mechanical impact
secondary-edema, exocytoxicity, inflammation, alterations in blood flow and metabolism
general disease course
- head trauma open vs closed
- loss or altered consciousness
- immediate CT scan; moderate to high risk pts
- conservative or surgical intervention; decompression, craniotomy
- most recovery within 6 mos
- coma state chronic disability and cont’d recovery/rehab
S/S of early TBI
headache concentration amnesia dizziness, nystagmus, balance nausea and vomiting seizures LOC, altered
S/S of late TBI
coma-common residual disability, recovery may occur
cognitive impairment-memory, attention, concentration; mental processing; impulse control and executive functions; personality
focal neurological signs
coma
pathophysiology-disturbance of function of brain stem reticular activating system (above mid-pons) or damage to both cerebral hemispheres
continuum between full alertness and deep coma
coma time line
lethargy to obtundation (mild-mod blunting of senses) to stupor to coma
sleep like state
- seemingly awake, but silent and motionless
- no purposeful response to environment
- reflex movements to stimulation
persistive vegetative state
- may last mos to yrs
- brain stem reflexes intact
- no purposeful movements
posturing reflexes
damage to descending pathways
- flexor (decorticate): midbrain and up
- extensor (decerebrate): midbrain and lower
Glasgow Coma Scale (GCS)
response category I. eye opening II. verbal response III. motor response low score= low prognosis
Closed brain injuries
- skull and dura mater remain intact
- most TBI result from closed head injuries
- contusion
- hemorrhage
- hematomas
open brain injuries
- penetrating
- fx or breach of skull and dura
- control of infection is critical
- contusion
- hemorrhage
diffuse axonal injury
- traumatic coma lasting >6 hrs caused by multiple small lesions in WHITE MATTER TRACTS
- axonal shearing injuries: axons stretched by high mechanical forces acting on head
- microscopic and macroscopic damage (tissue tearing in periventricular)
- mild DAI: 6-24 hrs
- mod to severe DAI: >24 hrs
- single most important cause of persistent disability after TBI
cerebral contusion and hemorrhage
- bruising of the brain
- focal parenchymal traumatic lesion, especially in elderly
- coup and contrecoup lesions (opposite pole of impact)
- hemorrhage: intracerebral, subdural
common sites for contusions
- inferior frontal lobe
2. temporal lobe
hematoma
focal collections of blood clot that displace the brain
- epidural: convex bulging (blood pooling, duramater)
- subdural: classic crescent shape
acute subdural hematoma
- stretching and tearing of the bridging veins that drain into sinuses (sometimes arterial)
- typically associated with severe head injury (falls and assaults)
- symptomatic within 72 hrs of injury
- half experience a LOC at injury
chronic subdural hematoma
- fibroblasts on inner surface of dura form thick outer membrane
- inner thin membrane develops, encapsulating the clot, then liquefies
- slow developing symptoms (headaches, change in mental status)
- elderly
- often recurrent episodes of bleeding and clotting
epidural hematoma
- usually tear in wall of meningeal artery
- bulging convex pattern on CT
- majority associated with skull fxs
- young adults
- leads to severe brain damage
CT scan, appearance of blood depends on it’s age
acute blood: hyperdense (bright)
after 1-2 wks: clot begins to liquefy, isodense
after3-4 wks: clot is completely liquefied, hypodense (dark)
concussion
- a direct blow to head
- alteration of consciousness is brief (
long-term concussion consequences
post-concussion syndrome
second impact syndrome
chronic traumatic encephalopathy
post-concussion syndrome
persistence of headache, dizziness, fatigue, insomnia, other symptoms
may last wks, mos, or even yrs
second impact syndrome
rare reports of severe brain swelling after a second blow to the head after an initial concussion
chronic traumatic encephalopathy
- progressive deteriorization of neural tissue
- cumulative effects of of multiple concussions
- inc risk of Alzheimer disease and other cognitive impairments
- symptoms: depression, aggressive behavior, impulse control issues, and memory
concussion management in sports
on-field assessment- SCAT3
later evaluation in ER of office
graded return to physical activity protocol
children
risk stratification
low: normal neurological exam, no concussion
mod: failure reach GCS 15 w/in 2 hrs; concussion, seizure, vomit
high: GCS scores 3-8; focal neurological signs
treatment of epidural hematoma and acute subdural hematoma
surgical decompression and management of intracranial pressure
treatment of chronic subdural hematoma
surgical evacuation of large hematomas; small hematomas may be manages conservatively
