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Neuro Unit 2 > CNS Injury > Flashcards

CNS Injury Flashcards

1
Q

What percentage of head injury deaths occur prior to hospitalization

A

66%

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2
Q

What is the peak age group for head injury?

A

25-35

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3
Q

Name the most common cause of TBI

A

Falls, Struck by/against, Motor vehicle traffic, Assault

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4
Q

Name some forces resulting in cerebral trauma

A

Contact, Acceleration (translational, rotational), Penetrating, Second Injury

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5
Q

When is the peak for fall related head injuries?

A

Over age 65

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6
Q

When is the peak for child abuse related head injuries?

A

Age 0-4

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7
Q

What are the local effects of contact phenomena

A

scalp lacerations, subgaleal hematomas, skull fractures, epidural hematomas

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8
Q

What are the four types of skull fractures?

A

linear, depressed, basilar, and growing

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9
Q

What is the significance of basilar fractures?

A

Can cause issues with cranial nerves and with csf leak leading to meningitis

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10
Q

What is a growing fracture?

A

When a young chid gets a skull fracture, it may cause the dura to tear and arachnoid mater comes out as the bone pops back out, and the pulsation of CSF against the skull causes resorption of the bone.

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11
Q

What is an issue with a depressed fracture?

A

It can press in and injure whatever brain tissue is there

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12
Q

What are the clinical signs of skull base fracture?

A

CSF leak from nose or ears, raccoon eyes (hours after injury), bleeding from ear, facial nerve palsy, battle sign (bruise look behind ear 12-24 hours later)

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13
Q

What is the classic ‘lucid interval’ associated with epidural hematomas?

A

Patient appears to be neurologically normal after they wake up from the concussion, but then lose consciousness several hours later

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14
Q

What causes epidural hematomas?

A

Contact injury with skull fracture that disrupts an artery within the groove of the skull

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15
Q

What does translational injury cause?

A

stretching and tearing of the veins between the brain and the dura

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16
Q

What are coup and countercoup injuries?

A

Coup injury is the injury from impact against object. Countercoup is the impact within the skull on the opposite side from whiplash.

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17
Q

How can you differentiate between subdural and epidural hematoma?

A

The shape of the hematoma. More spread out with subdural, and more lens-like with epidural

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18
Q

Why is a subdural hematoma more fatal

A

A lot of energy was imparted to the brain from the original injury, and then the pressure from the hematoma is compounding the issue.

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19
Q

What are rotational injuries?

A

The brain rotates within skull- usually associated with motor vehicle ejections, being struck by a car, motorcycle accident

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20
Q

What are the effects of rotational injuries?

A

Microscopic tearing of the nerve cell in the brain- diffuse axonal injury leading to retraction balls. MRI studies often show punctuate hemorrhages in large white matter tracts such as the corpus callosum, and near the grey-white junction

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21
Q

What is chronic traumatic encephalopathy immunohistochemically related to?

A

Alzheimer’s disease

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22
Q

What histological changes might be seen with diffuse axonal injury?

A

axonal spheroids

23
Q

How is an increase in intracranial volume accomodated

A

decreases in CSF or CBV

24
Q

Where is CNS blood volume displaced?

A

Jugular venous system

25
Q

Where is CNS CSF displaced?

A

Spinal subarachnoid space

26
Q

What happens when the maximum compensatory mechanisms for ICP are exhausted

A

Small increases in volume of a mass can produce marked elevations in ICP and lead to ischemia if ICP is greater than arterial pressure. CPP=MAP-ICP. Ischemia leads to energy failure, and more cytotoxic and vasogenic edema.

27
Q

What are the different types of herniation caused by ICP increase?

A

Lateral (cingulate herniation- can kink anterior cerebral arteries), Medial (transtentorial/uncal herniation can push on the midbrain or kink posterior cerebral artery), Tonsilar herniation (leads to compression of the medulla that can cause a spike in blood pressure that leads to bradychardia- Cushing’s sign)

28
Q

What are some symptoms that are concerning for uncal herniation?

A

Ipsilateral blown pupil and contralateral hemiparesis

29
Q

What kind of contusions are caused in the brainstem by herniation?

A

Duret hemmorhage

30
Q

What causes brain swelling?

A

Mechanical forces of TBI cause widespread depolarization and NT release, leading to increased CBF, disrupting autoregulation of CBF

31
Q

What can result from loss of vessel autoregulation in CNS?

A

hyperemia or ischemia

32
Q

What is the mechanism of cerebral edema?

A

The glutamate transporter on the astrocyte releases glutamate, rather than taking it up- rapid increase in calcium at postsynapic terminal is toxic and leads to cell death Potassium level rises rapidly and leads to even greater glutamate release. ????????????????????????????????????????????????????????

33
Q

How do you treat traumatic brain injury at the scene?

A

Prevent hypoxia and hypotension: Airway patency, Breathing, Circulation

34
Q

What is the treatment after stabilization?

A

Reduce ICP:

1) Mannitol (osmotic)
2) Ventricular drain

35
Q

Why should you avoid spinal tap in a patient with elevated ICP?

A

Can lead to herniation

36
Q

How do you assess a patient with TBI (comatose/unconscious)?

A

Measures of eye, motor, and verbal response

37
Q

What are the important brainstem reflexes?

A

Pupillary reflex (CN 2,3, midbrain)
Corneal blink reflex (CN 5, 7, pons)
Cold Caloric Testing (oculocephalic response- CN 8, 6, 3, pons, midbrain)- bobbing of the eyes toward the side with the cold water
Gag, cough reflexes (CN 9, 10, medulla)

38
Q

What are predictors of mortality in TBI

A

GCS and blood pressure

39
Q

Define concussion, or mild traumatic brain injury

A

An alteration in mental status caused by mechanical forces that may or may not cause loss of consciousness. The most common symptoms include h/a, dizziness, poor attention, inability to concentrate, memory problems, fatigue, irritability, depressed mood, intolerance of bright
light or loud noise, and sleep disturbance. Region of brain affected is usually limited to the grey/white junction immediately beneath the cortex.
Colorado concussion grading:
Grade 1: confusion without amnesia or LOC
Grade 2: confusion with amnesia
Grade 3: LOC

40
Q

What are the effects of a subfalcian herniation?

A

The cingulate gyrus herniates and can obstruct the anterior cerebral artery, causing ischemic events in that distribution

41
Q

What are the effects of an uncal herniation?

A

Can put pressure on the midbrain and its ipsilateral cerebral peduncle, leading to ipsilateral third nerve palsy and contralateral hemiparesis or hemiplegia.
Can also cause a duret hemorrhage (disrupts ascending reticular activating system)

42
Q

What is Kernohan’s notch?

A

Rare condition in which the uncal herniation compresses the contralateral cerebral peduncle, leading to ipsilateral hemiparesis or hemiplegia

43
Q

What are the effects of a central herniation?

A

Can cause bilateral uncal herniation

44
Q

What are the effects of a tonsilar herniation?

A

Midbrain is compressed, leading to abnormal cardiac and respiratory responses, including Cushing’s reflex- bradycardia and hypertension in the setting of high ICP.
Usually occurs due to mass lesion in the posterior fossa

45
Q

What is the clinical manifestation of herniation?

A

Abrupt change in neurological function.

Often pts will experience h/a, nausea, vomiting, then progressive lethargy and eventual loss of consciousness

46
Q

Explain the mechanism of excitotoxicity

A

After an injury, there is widespread depolarization, which causes a huge increase in extracellular Potassium. This causes a reversal of the Glutamate transporter, so that there is no reuptake of Glutamate in the synapse. The glutamate binds to NMDA and AMPA receptors, increasing intracellular levels of calcium to toxic levels, such that they cause the release of phospholipases, endonucleases, and proteases such as calpain. These enzymes damage the cells, but they also damage the blood-brain barrier, leading to vasogenic edema. On top of this, the astrocyte is trying to take up te abundance of potassium and starts to swell, putting additional pressure on the capillaries because the astrocyte foot processes abut them. This combined with vasogenic edema results in reduced blood flow to the brain and ischemia that leads to further failure of ATPases, so the Na/K pump cannot keep the neuron hyperpolarized.

47
Q

How should elevated intracranial pressure be treated?

A

Immediate intubation for all unconscious patients, hyperventilation to reduce CO2 can be done transiently to vasoconstrict the vessels of the brain, elevation of the head of the bed to increase venous return, mannitol to create an osmotic and oncotic gradient, ventricual catheters to drain CSF spaces if hydrocephalus is present, drug induced coma with barbiturates to reduce metabolic demand of the brain and scavenge free radicals.

48
Q

What is second impact syndrome?

A

If a second concussion occurs while still suffering the effects of a previous one, there is a loss of autoregulation of CNS vasculature. Cerebral vessels lose tone and become clogged with blood, leading to increased ICP and decreased perfusion- widespread ischemia and vasogenic edema. Usually fatal.

49
Q

Identify the peak age groups in which head injuries occur and the mechanisms whereby these injuries are received

A

0-4 child abuse
24-35 transport, gunshot wounds, falls, and non-penetrating assaults
65+ falls

50
Q

Discuss the pathophysiology of various types of head injury and how they occur

A

1) contact - can lead to lacerations of the scalp, fractures of the skull, epidural hemorrhage/hematoma, and cerebral contusions
2) acceleration/deceleration- can create cerebral contusions and subdural hematomas hemorrhages

51
Q

What are the effects of diffuse axonal injury?

A

Depending on the severity and extent of injury, these changes can manifest acutely as immediate loss of consciousness or confusion and persist as coma and/or cognitive dysfunction. In addition, recent evidence suggests that TBI may induce long-term neurodegenerative processes, such as insidiously progressive axonal pathology.

52
Q

Recognize the Glasgow Coma Scale, its utility in predicting injury severity and outcome, and the elements of the clinical evaluation of concussion

A

Measures eye opening, motor response, and verbal response, then risk stratifies based on results. High GCS corresponds with more minor TBI and predicts better long term outcome.

53
Q

List five of the most common symptoms of concussion

A

h/a, dizziness, poor attention, inability to concentrate, memory problems

Neuro Unit 2 (21 decks)

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