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Neuro Pathology > Brain Injury > Flashcards

Brain Injury Flashcards

1
Q

CNS vs PNS

A

CNS

  • UMN: cortical, brainstem
  • other: basal ganglia, cerebellum, other
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2
Q

Brain Injury causes

A

-falls 36%
-MVA 26%
-objects 24%
-assault 14%
sports-related TBI is 2nd only to MVA

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3
Q

pediatric TBI

A
  • most common cause of physical disability can cognitive impairment in young people
  • MOI: MVA or isolated pediatric head injury
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4
Q

Neuroanatomy

A
  • layer of protection: meningeal layers

- anterior, middle, and posterior fossae and contents

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5
Q

tenorium cerebelli

A

differentiates supra (cortex) and infra (cerebellum) tentorium regions

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6
Q

tentorial notch

A

where a herniation can occur

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7
Q

types of pathogenesis

A 
axonal shearing
cerebral contusions and hemorrhage
subdural hematoma
epidural hematoma
concussion
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8
Q

Primary vs secondary injury

A

primary-mechanical impact

secondary-edema, exocytoxicity, inflammation, alterations in blood flow and metabolism

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9
Q

general disease course

A
  • 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
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10
Q

S/S of early TBI

A 
headache
concentration amnesia
dizziness, nystagmus, balance
nausea and vomiting
seizures
LOC, altered
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11
Q

S/S of late TBI

A

coma-common residual disability, recovery may occur
cognitive impairment-memory, attention, concentration; mental processing; impulse control and executive functions; personality
focal neurological signs

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12
Q

coma

A

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

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13
Q

coma time line

A

lethargy to obtundation (mild-mod blunting of senses) to stupor to coma

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14
Q

sleep like state

A
  • seemingly awake, but silent and motionless
  • no purposeful response to environment
  • reflex movements to stimulation
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15
Q

persistive vegetative state

A
  • may last mos to yrs
  • brain stem reflexes intact
  • no purposeful movements
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16
Q

posturing reflexes

A

damage to descending pathways

  • flexor (decorticate): midbrain and up
  • extensor (decerebrate): midbrain and lower
17
Q

Glasgow Coma Scale (GCS)

A 
response category
I. eye opening
II. verbal response
III. motor response
low score= low prognosis
18
Q

Closed brain injuries

A
  • skull and dura mater remain intact
  • most TBI result from closed head injuries
  • contusion
  • hemorrhage
  • hematomas
19
Q

open brain injuries

A
  • penetrating
  • fx or breach of skull and dura
  • control of infection is critical
  • contusion
  • hemorrhage
20
Q

diffuse axonal injury

A
  • 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
21
Q

cerebral contusion and hemorrhage

A
  • bruising of the brain
  • focal parenchymal traumatic lesion, especially in elderly
  • coup and contrecoup lesions (opposite pole of impact)
  • hemorrhage: intracerebral, subdural
22
Q

common sites for contusions

A
  1. inferior frontal lobe

2. temporal lobe

23
Q

hematoma

A

focal collections of blood clot that displace the brain

  • epidural: convex bulging (blood pooling, duramater)
  • subdural: classic crescent shape
24
Q

acute subdural hematoma

A
  • 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
25
Q

chronic subdural hematoma

A
  • 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
26
Q

epidural hematoma

A
  • usually tear in wall of meningeal artery
  • bulging convex pattern on CT
  • majority associated with skull fxs
  • young adults
  • leads to severe brain damage
27
Q

CT scan, appearance of blood depends on it’s age

A

acute blood: hyperdense (bright)
after 1-2 wks: clot begins to liquefy, isodense
after3-4 wks: clot is completely liquefied, hypodense (dark)

28
Q

concussion

A
  • a direct blow to head

- alteration of consciousness is brief (

29
Q

long-term concussion consequences

A

post-concussion syndrome
second impact syndrome
chronic traumatic encephalopathy

30
Q

post-concussion syndrome

A

persistence of headache, dizziness, fatigue, insomnia, other symptoms
may last wks, mos, or even yrs

31
Q

second impact syndrome

A

rare reports of severe brain swelling after a second blow to the head after an initial concussion

32
Q

chronic traumatic encephalopathy

A
  • 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
33
Q

concussion management in sports

A

on-field assessment- SCAT3
later evaluation in ER of office
graded return to physical activity protocol
children

34
Q

risk stratification

A

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

35
Q

treatment of epidural hematoma and acute subdural hematoma

A

surgical decompression and management of intracranial pressure

36
Q

treatment of chronic subdural hematoma

A

surgical evacuation of large hematomas; small hematomas may be manages conservatively

Neuro Pathology (7 decks)

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