CNS Trauma I, II, III (Ojemann, Breeze, Kelly) Flashcards

1
Q

What populations are at highest risk for traumatic head injury?

A
  • ->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.
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2
Q

What defines a contact injury? What type of injury can result.

A

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

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3
Q

Penetrating injuries

A

Penetrate the skull and dura (gunshot wounds do a lot better than you think, particulary if the bullet doesn’t cross the midline

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4
Q

What defines an acceleration impact? What types of injury result from acceleration?

A

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)

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5
Q

Skull fractures (4 types)

A

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

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6
Q

Clinical signs of Basilar fracture (low yield?)

A

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

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7
Q

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?

A

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)

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8
Q

Subdural Hematomas

A

High mortality relative to the epidural hematoma
Primary Injury to the brain itself
More “crescent” shaped

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9
Q

With what type of trauma are cerebral contusions formed? What is the prognosis?

A

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)

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10
Q

What defines a rotational injury? What types of accidents cause this trauma?

A

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).

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11
Q

What defines Diffuse Axonal Injury? What might be visible on CT/MRI? What other histological evidence can be seen, and what is the timeframe?

A

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.

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12
Q

What methods of compensation does the brain have to deal with changes in ICP?

What happens when compensation is maxed out?

A

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.

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13
Q

Describe the spectrum of rotational injury.

A

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).

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14
Q

SCALP mnemonic

A
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.

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15
Q

Name the 4 types of intercranial herniation.

A
  1. Subfalcine (cingulate) - ACA ischemia
  2. Central
  3. Uncal - PCA ischemia
  4. Tonsilar

**These are described in subsequent flashcards.

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16
Q

Describe a subfalcine herniation. What are the risks/consequences?

A

The cingulate gyrus is pushed underneath the falx cerebri. The anterior cerebral a. is often kinked, leading to a stroke.

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17
Q

Describe a transtentorial (uncal) herniation. What structures are compressed, and what are the symptoms of each?

A

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.

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18
Q

What is central herniation (3 words)?

A

Bilateral uncal herniation.

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19
Q

Describe tonsillar herniation. What are the symptoms? What is the most common cause?

A

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.

20
Q

What is Cushing’s reflex?

A

Bradycardia and hypertension in the setting of increased ICP.

21
Q

What is excitotoxicity?

What series of steps leads to vasogenic edema?

A

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.

22
Q

Differentiate vasogenic from cytotoxic edema.

A

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.

23
Q

Even before excitotoxic injury can occur, the widespread simultaneous neuronal depolarization results in an immediate spike in extracellular K+. What happens next?

A

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.

24
Q

What are 4 pathophysiologic changes seen in TBI (broad, synthesis card)?

A

Brain swelling–> reduced perfusion (ischemia)
Loss of autoregulation–> areas of overperfusion
Cytotoxic edema
Vasogenic edema

25
Q

What is the very general principle guiding treatment of increased ICP? What are some specific interventions mentioned in the lecture?

A

Manage ABCs (MUST intubate)

Can also: Mannitol, ventricular catheter, reduce pCO2 (somehow decreases blood volume due to vasoconstriction?), elevate head, induce coma with barbituates (reduced metabolic demand, scavenge free radicals).

26
Q

What is a normal cranial perfusion pressure? What is the formula used to calculate it?

A

CPP = MAP - ICP

MAP = 80
ICP (normal) = 10
CPP (normal) = 70

27
Q

What are the ranges (normal/slight increase/moderate increase/severe increase) of ICP?

A
Normal = 3-15 mHg
Slight = 16-20
Moderate = 21-40
Severe = 40+
28
Q

What is the pupillary reflex? What nerves are checked, and what part of the brain? What is a normal response?

A

Shine a light on one eye, contralateral eye should also constrict (both together, to the same degree).

Checks CN 2,3 and the midbrain

29
Q

What is the corneal reflex? What nerves are checked, and what part of the brain? What is a normal response?

A

Touch the cornea, both eyes should blink simultaneously.

Checks 5, 7 and the pons.

30
Q

What is the “doll’s eye” test?

A

Rock the patient’s head side to side. A normal response is that the eyes look straight ahead.

31
Q

What is “cold caloric” testing?

A

Don’t do to friends…they will puke:)

Flush cold water through one ear, should see nystagmus.

32
Q

What nerves and brain area does the gag reflex check?

A

CN 9, 10 and the medulla

33
Q

What are the 6 motor checks on the GCS? How many pts are awarded for each?

A

6 - obeys commands
5 - localizes pain (eg hand crosses midline)
4 - flexion (pulls hand away)
3 - abnormal flexion (decorticate - palsy-like)
2 - extension (decerebate - stiffens)
1 - none
(lowest score = 3, highest = 15)

34
Q

What is “second impact” syndrome relative to concussion?

A

There is an apparent loss of autoregulation of the CNS vasculature such that cerebral vessels loose tone and become congested with blood. Intracranial pressure rises as intravascular volume increases, reducing cerebral perfusion that leads to widespread ischemia and vasogenic edema. Once the process has begun, it is virtually impossible to halt.

35
Q

What are the symptoms of concussion?

A

The hallmarks of concussion are confusion and amnesia.

Others: headache, dizziness, poor attention, inability to concentrate, memory problems, fatigue, irritability, depressed mood, intolerance of bright light or loud noise, and sleep disturbance.

36
Q

What are the early symptoms (not signs) of concussion?

A
Confusion
Headache
Lack of awareness of surroundings
Dizziness, vertigo
Nausea, vomiting
37
Q

What are the late signs of concussion (persistent signs)?

A
Persistent headache
Lightheadedness
Decreased attention and concentration
Poor memory
Easy fatigability
Irritability
Anxiety or depressed mood
Sleep disturbance

**Sleep disturbance has to be treated. This is the one thing we have going that could be considered a treatment. W/o sleep you will have all the rest

38
Q

What are signs (not symptoms) of concussion?

A

VACANT STARE (dazed, befuddled facial expression)
DELAYED RESPONSES (slow to answer questions or follow instructions)
INATTENTION (easily distracted or unable to track conversations)
DISORIENTATION (walking in the wrong direction, unaware of time, date, place)
SLURRED OR INCOHERENT SPEECH (making disjointed or incomprehensible statements)
INCOORDINATION (stumbling, inability to walk tandem/straight line)
INAPPROPRIATE EMOTIONALITY (appearing distraught, crying for no apparent reason)
MEMORY PROBLEMS (exhibited by athlete repeatedly asking a question that has already been answered or exhibiting memory deficits on mental status testing)
LOC (paralytic coma, unresponsiveness to stimuli)

39
Q

What is responsible for contralateral brain damage in the classic “coup/contrecoup” injury?

A

Cavitation. [vacuum effect with bubble formation – bubbles decompress as soon as the brain resettles but damage is done. IN the example in class, a hematoma resulted from the contrecoup]

40
Q

Regardless of the direction/location of the force, the ___ and ___ lobes are the most severely affected.

A

Frontal and temporal

41
Q

What are the 3 big pathophysiological steps in concussion?

What also contributes

A

1) Shearing forces and wave propagation leads to massive depolarization throughout the cortex
2) excessive neurotransmitter release, driving up cellular metabolism rates and lactic acid levels
3) Na/K pump failure and disruption of axonal transport lead to electrolyte imbalances and axonal swelling/disintegration

Rotational forces also cause shearing of the blood supply (capillaries) which contributes to damage.

42
Q

What happens to glucose metabolism in a concussed brain?

A

It resembles the brain of someone in a persistent coma. Eg PET scanning turns blue instead of red/green (very little metabolism).

43
Q

If petechial hemorrhages are present on someone with symptoms of concussion, what can be assumed?

A

IF BV are broke (hemosiderin/petechial hemorrhages) you KNOW the axons are damaged b/c they are more fragile. IF you see this = TBI (argument is that this shouldn’t be considered mild but rather serious injury)

Black spots are iron (hemosiderin). Lesions are near the grey/white junction. Differing densities (banana/jello analogy).

44
Q

Is amnesia associated with LOC?

A

Trick question.

Yes. LOC = amnesia.

However, amnesia can occur with no LOC (troy aikman).

45
Q

Do people with more severe symptoms take longer to recover and have higher likelihood of sequelae?

A

Yes. The period of rest should be determined by the duration of symptoms. Seems like 7 days is a minimum.

46
Q

What is the pathophysiology of second-impact syndrome?

A

People literally collapse unconscious after 1 hit. From lecture notes of CT scan with diffuse white signal:

[This is an abnormal scan. The ventricles are too large for 18 y/o. The whiteness around the brain ( in the tissue) was way too much. Was though to be SAH. Turns out it was blood, but wasn’t in the subarachnoid space. What happens under these cirucmstances after 2 concussions (or severe brain injury) there is autoregulatory failure of bv more in the venous end than arterial. The brain literally swells. This happens before edema even has a chance to leak out of the capillaries. The distended veins raise ICP (in this patient was 56. Below 20 is normal)].

47
Q

Aside from the motor checks, what other two categories exist in the GCS?

A

Eye opening (spontaneous, to speech, to pain, none)

Verbal response (Oriented, confused, inappropriate words, incomprehensible sounds, none)