CNS Trauma

Question 1

Common concussion symptoms

Answer 1

Confusion, amnesia, headache, dizziness, poor attention, inability to concentrate, irritable, fatigued, depressed, intolerant of bright light/loud noise, sleep disturbance

Question 2

leading cause of death up to age 45?

Answer 2

trauma

Question 3

Grading scales

Answer 3

no universal scale

Question 4

Colorado Concussion Grading Scale

Answer 4

Grade 1: confusion/no amnesia or LOC
Grade 2: Confusion + amnesia
Grade 3 - LOC

Question 5

Second Impact Syndrome

Answer 5

Rare; consequence of second concussion while still having effects of first. loss of autoregulation of CNS vasculature that cerebral vessels lose tone and get congested with blood –>increased ICP –> reduced perfusion (ischemia, vasogenic edema); almost impossible to halt process once started

Question 6

concussion

Answer 6

mild TBI; alteration i mental status due to biomechanical forces that may/may not cause LOC

Question 7

Concussion management

Answer 7

Observe 24 hrs; no need to wake pt at night unless anmesia/unconsciousness; acetominophen for pain

Gradual return to activities and different therapies if needed

Question 8

Peak age groups for head injuries

Answer 8

25-35
Males 2x as likely (4x fatality risk)
small peaks in 0-4 (abuse) and >65 (falls)
Highest incidence in economically disadvantaged populations within major cities

Question 9

Principle forces of injury in cerebral trauma

Answer 9

1. Contact (object striking head)
2. Acceleration/deceleration(rapid head movement that can create shear, tensile, compressive strains; DON’T need to involve impact) – translation vs rotational
   - Results in stretching/tearing of veins between brain and dura and bruising of brain as it impacts skull
3. Penetrating (GSW, knives, tree branches)
4. Secondary Injury

Question 10

Primary injury

Answer 10

Injury at moment of impact; little regeneration of neural tissue; largely irreversible injury

Question 11

Secondary injury

Answer 11

Due to inadequate reuscitation (hypoxia, dysautoregulation, released of free radicals that break down BBB –> interstitial edema)

Question 12

Injuries due to contact phenomena

Answer 12

scalp lacerations, skull fractures, cerebral contusion, epidural hematoma, subgaleal hematoma

Question 13

Injuries from Acceleration/Deceleration

Answer 13

Diffuse axonal injury, cerebral contusion, subdural hematoma

Question 14

Excitotoxicity

Answer 14

pathological process where neurons are damaged/killed by overactivation of receptors for glutamate. This causes increased Ca inside cell that activates enzymes that damage cell structures and BBB—> Vasogenic edema

Question 15

Cytotoxic edema

Answer 15

due to high K outside cell that causes glutamate transporter to reverse and pump more K into cell. Leads to cell swelling and thus brain swelling.

Question 16

Treating elevated ICP

Answer 16

minimize ICP/maximize oxygen and metabolite delivery

Question 17

Emergency measures to treat ICP

Answer 17

IV osmotic diuretics, ventricular catheters, treat obstructive hydrocephalus, drug-induced coma with barbituates, elevate head, controlled CO2 ventilation

Question 18

Monroe-Kellie doctrine

Answer 18

Intracranial compensation for expanding mass; allows you to compensate and retain normal ICP up to a point.

Brain in rigid container; increase volume of mass of one compartment will increase the pressure unless there is a compensatory decrease in volume of another compartment

Volume of intracranial compartment = volume FSC + blood volume in arterial/venous systems+ brain + intracranial mass lesion = constant volume. To keep pressure, maintain volume.
Increase pressure too much, have compression of compartments. Some elements more compressible than others

Question 19

Intracranial compensation

Answer 19

Brain is essentially noncompressible. Increase in ICV decreases CSF or cranial blood volume, and CSF wlil displace into spinal subarachnoid space and venoconstriction of CNS capacitance vessels displaces blood in jugular venous system

Question 20

Herniation

Answer 20

ICP increases not distributed equally in skull, so you have pressure gradients that cause parts of brain to herniate.

Types – subfalcine, central, uncal (transtentorial), tonsillar

Question 21

Lateral/Subfalcine herniation

Answer 21

cingulate gyrus eing pushed by expanding mass and herniates under falx cerebri; often kinks anterior cerebral artery to potentially cause stroke in the distribution of that vessel

Question 22

Central herniation

Answer 22

downard pressure centrally can cause bilateral uncal herniation below tentorium cerebrlli

Question 23

Uncal herniation

Answer 23

Uncus herniates across tentorial edge, and downward into posterior fossa.

Compression of midbrain/ipsilateral cerebral peduncle–> usually produces ipsilateral third nerve palsy and contralateral hemiparesis/hemiplegia.

Rarely compresses contralateral cerebral peduncle against tentorial edge to cause hemiparesis ipsilateral to mass lesion/herniated uncus –> this is called Kernohan’s notch

Can also produce Duret hemorrhage

Question 24

Kernohan’s notch

Answer 24

phenomenon when uncal herniation causes contralateral cerebral peduncal to compress against tentorial edge, resulting in hemiparesis ipsilateral to mass lesion/herniated uncus

Question 25

Duret hemorrhage

Answer 25

uncal herniation causes hemorrhage in brainstem –> produces disruption in ascending reticular activating system that can lead to devastating neurologic consequences

Question 26

Tonsillar herniation

Answer 26

cerebellar tonsilsherniate down tinto foramen magnum (“coning”).

Question 27

Cushing’s reflex

Answer 27

bradycardia and hypertension in setting of high ICP

Tonsillar herniation compresses the medulla that can produce abnormal cardiac/respiratory responses, including Cushing’s reflex

Question 28

Glasgow Coma Scale

Answer 28

well-validated, straightforward scale that correlates with likelihood pt harbors intracranial mass lesion and with likelihood of good outcome, moderate disability, severe disability, or death.

Good interobserver reliability; measure best response

Question 29

Brainstem reflexes

Answer 29

Pulillary, Corneal blink reflex, cold caloric testing, gag reflex

Question 30

Pupillary refles

Answer 30

CN 2, 3, midbrain

Question 31

Corneal blink reflex

Answer 31

CN 5, 7, Pons

Question 32

Cold caloric testing

Answer 32

“Doll’s Eyes”; CN 8, 6, 3, pons –> midbrain

Question 33

Gag reflex

Answer 33

CN 9, 10 medulla

Question 34

Cerebral Contusion

Answer 34

acceleration injury: translational; frontal/temporal injuries; may see swelling, brain shift, increased ICP, herniation; low mortality

Question 35

Coup and Countrecoup injury

Answer 35

coup injury against object; countrecoup injury - impact within skull

example: head strikes wall (coup) and then rebounds (countrecoup)

Question 36

subdural hematoma

Answer 36

acceleration – translational; rupture of bridging veins in subdural space

associated with contusions
high mortality rate

Question 37

Acceleration – rotational injury

Answer 37

Due to head moving in more than one plane (motor vehicle ejection, motorcycle accident)

Results in microscopic tearing of nerve cells in brain. No recognizable injury detected without a microscope

Diffuse axonal injury

Question 38

Signs of Skull Base fracture

Answer 38

CSF Rhinorrhoea, bilateral periorbital haematomas (Racoon eyes), subconjunctival haemorrhage, bleeding from external auditory meatus, CSF otorrhoea, Battle’s sign, Facial nerve palsy

Question 39

Epidural hematomas

Answer 39

contact phenomena; intracranial extradural arterial hemorrhage

associated with skull fractures
Classic “lucid interval”
low mortality rate

Question 40

TBI

Answer 40

Mechanical forces cause widespread depolarization and NT release –>