CNS Trauma I, II, III (Ojemann, Breeze, Kelly) Flashcards
What populations are at highest risk for traumatic head injury?
- ->Highest incidence occurs in economically disadvantaged populations within major cities (240-400/100,000 population).
- ->Males are at twice the risk of brain injury as females and are as much as 4 times the risk for fatal injuries.
- ->The peak age range is 24-35 with small peaks at 0-4 years for child abuse and over 65 years for falls at home.
What defines a contact injury? What type of injury can result.
Lower velocity (bats, rocks, bottles)
Damage to the protective coverings of the brain, often don’t damage the brain.
Scalp lacerations, subgaleal hematomas, epidural hematomas, skull fractures
Penetrating injuries
Penetrate the skull and dura (gunshot wounds do a lot better than you think, particulary if the bullet doesn’t cross the midline
What defines an acceleration impact? What types of injury result from acceleration?
Higher velocity injury from head movement in a single plane the instant after impact (windshield, fall etc)
Results in 1) stretching and tearing in the veins (subdural hematoma) and 2) bruising of the brain (contusions)
Skull fractures (4 types)
Linear - straight line
Depressed - bone inward (often no tx needed)
Basilar - base of the skull (CSF leak, NG tube into brain)
Growing fracture (unusual - very rare) - Age 1-2 Hit head on coffee table, depresses along the suture, dura herniates through the suture, and the pulsations of CSF prevent bone growth requiring interventions
Clinical signs of Basilar fracture (low yield?)
CSF rinorrhea
CSF otorrhea
Bilateral periorbital hematomas (racoon eyes)
Battle’s sign (blood tracking behind the ear - 12 hr to show)
Facial nerve palsy
Subjunctival hemorrhage
What type of injury causes an epidural hematoma? What is the characteristic finding on imaging? What is the “classic” presentation? What is the mortality with treatment? What vessel(s) bleed?
Contact phemonenon - initial impact doesn’t damage brain, but the hematoma will if not treated appropriately, hence the relatively low mortality rate (20%)
Bleeding in the meningeal arteries
“Classic” lucid interval - knocked out, wake up, then become lethargic and go back under (exams…not often irl)
“lenticular shape” on CT due to tight adhesion of dura to skull (vs subdural which is more “crescent” shaped)
Subdural Hematomas
High mortality relative to the epidural hematoma
Primary Injury to the brain itself
More “crescent” shaped
With what type of trauma are cerebral contusions formed? What is the prognosis?
Caused by accelerational injury. Have low mortality, often have no major symptoms and can be treated conservatively.
Can result in more severe symptoms (swelling, brain shift, increased ICP, herniation)
What defines a rotational injury? What types of accidents cause this trauma?
Results from the head moving in multiple planes (moto, pedestrian vs car, etc)
Results in MICROscopic tearing of the nerve cells in the brain (no gross deformity notable).
What defines Diffuse Axonal Injury? What might be visible on CT/MRI? What other histological evidence can be seen, and what is the timeframe?
Impact knocks patient out immediately. Might see punctate hemorrhages in the white tracts near the grey/white junction. Patients may persist in a coma and have long-term cognitive dysfunction.
Axons that have little tears (physical injury) is visible on microscopic examination (axonal spheroids, aka the “retraction balls of Cajal”). **These only appear in COMAS lasting for more than 6 hours. Visible on LM after 24 hours. Spheroids only detectable after 24 hours, the spheroids are NOT visible on CT/MRI.
Additionally, long term degenerative processes may be induced, many of which resemble Alzheimer’s.
**concussion is thought to fall on the “mild” side of the DAI spectrum.
What methods of compensation does the brain have to deal with changes in ICP?
What happens when compensation is maxed out?
The brain is non-compressible (acutely) so losses in volume must come from CSF or CBV.
CSF - displaced into the spinal subarachnoid space
Blood - vasoconstruction of CNS resistance vessels pushes blood into the jugular system
When these systems are exhausted, small changes in ICP will have huge effects, including reduction of CBF, which creates a vicious cycle.
Describe the spectrum of rotational injury.
Spectrum: Diffuse axonal injury (severe) —> concussion (mild)
A concussion causes physiologic disruption of neurons (wave of depolarization) due to mild rotation, and more severe insults will cause axonal injury (physical disruption).
SCALP mnemonic
S: skin
C: Cutaneous connective tissue
A: (galea) aponeurosis (of frontalis muscle)
L: loose connective tissue
P: periosteum
**When you scalp someone you go underneath the galea.
Name the 4 types of intercranial herniation.
- Subfalcine (cingulate) - ACA ischemia
- Central
- Uncal - PCA ischemia
- Tonsilar
**These are described in subsequent flashcards.
Describe a subfalcine herniation. What are the risks/consequences?
The cingulate gyrus is pushed underneath the falx cerebri. The anterior cerebral a. is often kinked, leading to a stroke.
Describe a transtentorial (uncal) herniation. What structures are compressed, and what are the symptoms of each?
The medial temporal lobe herniates downward across the edge of the tentorium.
The MIDBRAIN and IPSILATERAL cerebellar peduncle are compressed resulting in an ipsilateral 3rd nerve palsy and contralateral hemiparesis.
**The contralateral side can occasionally be compressed, resulting in hemiparesis that is ipsilateral to the mass (Kernohan’s notch).
**Uncal herniation can also produce a characteristic hemorrhage in the brainstem, a Duret hemorrhage, which produces devastating neurologic consequences, because of disruption of the ascending reticular activating system.
What is central herniation (3 words)?
Bilateral uncal herniation.
Describe tonsillar herniation. What are the symptoms? What is the most common cause?
The cerebellar tonsils push downward through the foramen magnum. Symptoms include Cushing’s reflex (Bradycardia, HTN) as well as abnormal cardiac and respiratory responses due to compression of the brainstem.
**Tonsillar herniation is most commonly encountered in the setting of a “mass lesion” in the posterior fossa.
What is Cushing’s reflex?
Bradycardia and hypertension in the setting of increased ICP.
What is excitotoxicity?
What series of steps leads to vasogenic edema?
A pathological process in which neurons are damaged/killed overactivation of receptors (NMDA, AMPA) by glutamate.
High levels of glutamate cause high intracellular Ca levels, which activate all sorts of enzymes (phospholipases, endonucleases, and proteases such as calpain) which damage cell structures (membranes, cytoskeleton, DNA), and most importantly, the BBB which leads to vasogenic edema.
Differentiate vasogenic from cytotoxic edema.
Vasogenic edema - caused by disruption of the BBB due to high intracellular Ca levels
Cytotoxic edema - caused by astrocyte swelling due to high ECF K+ and reversal of the glutamate transporter.
Even before excitotoxic injury can occur, the widespread simultaneous neuronal depolarization results in an immediate spike in extracellular K+. What happens next?
Astrocytes cannot clear glutamate because the transporter requires high ECF Na and high ICF K (2Na in/1Kout/1Glu in) The transporter reverses, which 1) increases synapse glutamate perpetuating the cycle and 2) causes uptake of K which causes the astrocyte to swell, leading to cytotoxic edema.
What are 4 pathophysiologic changes seen in TBI (broad, synthesis card)?
Brain swelling–> reduced perfusion (ischemia)
Loss of autoregulation–> areas of overperfusion
Cytotoxic edema
Vasogenic edema
