TRAUMATIC HEAD SPINAL CORD INJURY AND RAISED ICP Flashcards Preview

MD2- Neuroscience Block > TRAUMATIC HEAD SPINAL CORD INJURY AND RAISED ICP > Flashcards

Flashcards in TRAUMATIC HEAD SPINAL CORD INJURY AND RAISED ICP Deck (29):
1

what is a concussion

clinical term. following a sudden change in momentum of the head--- describes instantaneous loss of consciousness, temporary respiratory arrest, and loss of reflexes.

2

what is the purpose of the Glasgow coma scale?

based on eye response, verbal response, and motor response it predicts the extent of head injury following head injury.

3

what is the leading cause of death in adults under 45yrs age in the West?

CNS injury son!!!!!!

4

distinguish penetrating injury from a closed injury

penetrating injury is direct disruption of brain tissues.

closed injury is movement and compression of closed vascular structures within bony confines

5

what are some secondary effects of traumatic brain injury

ischaemia, hypoxia, epilepsy, raised ICP, infection

6

what is the diff b/w open and closed skull fractures?

open fractures communicate with the surface. both are indicative of a high energy transfer injury

7

what is a comminuted skull injury?

involving splintering of skull bones

8

what is a primary presenting characteristic of patients who've suffered basal fractures?

bleeding/csf leak from nose and ears

9

contusions?

hemorrhagic necrosis

10

coup

at impact site

11

contre coup

occurs when head is not immobilized at time of injury and involves opposite side of brain as well (head bounces back and forwards)

12

stereotypic contusions?

can occur at base of brain when the brain rubs against a rough surface (inferior frontal lobe, inferolateral temporal lobe)

13

what becomes of old contusions?

macrophages come in and take away damaged brain tissue. Brain DOES NOT fibrose. -->end up with areas of depressed brain tissue.

Glyotic brain with areas of hemosederin left at site of injury.

14

laceration?

penetration by foreign body or skull fragments

15

missile injury?

kinetic energy imparted by a bullet is determined by the projectile velocity

16

where is a likely site of diffuse axonal injury ?

corpus collosum

17

long term effects of diffuse axonal injury?

cerebral cortex somewhat preserved, most damage notable in white matter areas (loss of volume), gliosis process

18

what is gliosis

nonspecific reactive change of glial cells in response to damage to CNS

proliferation or hypertrophy of several different types of astrocytes, microglia, and oligodendrocytes.

In its most extreme form, the proliferation associated with gliosis leads to the formation of a glial scar.

19

what are complications of cord compressive acute traumatic injury?

vertebral tissue crushing cord causes compression of local spinal cord. hemorrhagic cord tissue pushed into adjacent cord, causing further damage.-->may develop expanding lesion -->quadriplegia is extreme outcome in survival case

20

long term sequelae of brain trauma?

infection, raised ICP, hydrocephalus (enlarged ventricles), epilepsy, brain atrophy due to neuronal loss, abnormal deposition of Tau protein, chronic traumatic encephalopathy (AFL injury), diffuse deposition of of A-beta plaques in cortex

21

what role does Tao protein play in the brain?

proteins that stabilize microtubules. They are abundant in neurons of the central nervous system. help with transport of nutrients and essential supplies.
abnormal deposition can lead to 'tangling'.

22

how much blood and csf is present in the cranium?

approx 150mL of each.
400ml of CSF is produced and circulated through CNS per day on avg.

23

describe compensatory process/dynamic of raised ICP

expanding brain lesion or cerebral oedema causes blood and csf to be expelled from brain to maintain pressure.
At upper limit of expulsion ICP begins to rise, may see herniation of cranial contents thru dural openings.

24

potential causes of raised ICP?

hemorrhage, overproduction of CSF/failure to reabsorb CSF, infarction, infection, tumor, trauma, cerebral oedema

25

two main subtypes of cerebral oedema?

1. VASOgenic
-predominantly white matter
-disruption of BBB w increased vascular permeability
-responds to steroids

2. CYTOtoxic
-both gray & white matter
-increased intracellular fluid due to glial, neuronal or endothelial cell injury
-NOT steroid responsive

26

where is csf produced?

in choroid plexus, mainly in lateral ventricles

27

What are the main potential sites of CSF blockage

1. foramen of munro (lateral ventricles)
2.third ventricle
3.Aqueduct of sylvius (en route from 3rd to 4th ventricle)
4.foramen of luschka and magendie (recess of 4th ventricle)
5. basal cisterns/subarachnoid spaces

28

impact of subdural hematoma on the rest of the cranial structures?

compressed gyrus, distorted lateral ventricles/midline shift, displacement/ distortion of brain stem, subfalcine herniation of cingulate gyrus, transtentorial herniation of medial temporal lobe, OR the extreme:
transforaminal herniation of cerebellar tonsil through foramen magnum (patient dead!)

29

describe transtentorial herniation

temporal lobe being pushed through tentori celebelli opening.
squeezing cerebral hemisphere on the opposite side against the tentorium producing confounding symptoms