TRAUMATIC HEAD SPINAL CORD INJURY AND RAISED ICP

Question 1

what is a concussion

Answer 1

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

Question 2

what is the purpose of the Glasgow coma scale?

Answer 2

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

Question 3

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

Answer 3

CNS injury son!!!!!!

Question 4

distinguish penetrating injury from a closed injury

Answer 4

penetrating injury is direct disruption of brain tissues.

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

Question 5

what are some secondary effects of traumatic brain injury

Answer 5

ischaemia, hypoxia, epilepsy, raised ICP, infection

Question 6

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

Answer 6

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

Question 7

what is a comminuted skull injury?

Answer 7

involving splintering of skull bones

Question 8

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

Answer 8

bleeding/csf leak from nose and ears

Question 9

contusions?

Answer 9

hemorrhagic necrosis

Question 10

coup

Answer 10

at impact site

Question 11

contre coup

Answer 11

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

Question 12

stereotypic contusions?

Answer 12

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

Question 13

what becomes of old contusions?

Answer 13

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.

Question 14

laceration?

Answer 14

penetration by foreign body or skull fragments

Question 15

missile injury?

Answer 15

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

Question 16

where is a likely site of diffuse axonal injury ?

Answer 16

corpus collosum

Question 17

long term effects of diffuse axonal injury?

Answer 17

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

Question 18

what is gliosis

Answer 18

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.

Question 19

what are complications of cord compressive acute traumatic injury?

Answer 19

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

Question 20

long term sequelae of brain trauma?

Answer 20

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

Question 21

what role does Tao protein play in the brain?

Answer 21

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’.

Question 22

how much blood and csf is present in the cranium?

Answer 22

approx 150mL of each.

400ml of CSF is produced and circulated through CNS per day on avg.

Question 23

describe compensatory process/dynamic of raised ICP

Answer 23

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.

Question 24

potential causes of raised ICP?

Answer 24

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

Question 25

two main subtypes of cerebral oedema?

Answer 25

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

Question 26

where is csf produced?

Answer 26

in choroid plexus, mainly in lateral ventricles

Question 27

What are the main potential sites of CSF blockage

Answer 27

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

Question 28

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

Answer 28

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!)

Question 29

describe transtentorial herniation

Answer 29

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