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CNS trauma and concussion Flashcards

1
Q

What are the three major reasons for head trauma?

A
  • Motor vehicle accidents
    • Recreational accidents
    • violence
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2
Q

What is the most “at risk” population for CNS trauma?

A
  • Economically disadvantaged
    • Within major cities
    • Males 4X more likely
    • 24-35 peak incidence
    • Smaller peaks 4yo or under or 65 or older (abuse)
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3
Q

What are the two categories of non-missile head injuries?

A
  • Contact and acceleration/deceleration
    • Contact is from an object striking the head and cuases local lacerations, fractures, epidural hematomas and cerebral contusions
    • Accel/decel, shear, tensile and compressive strains
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4
Q

What are the different types of skull fractures?

A

• classified as linear, depressed, basilar, diastatic, and growing.

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5
Q

What do you worry about with a depressed skull fracture?

A

• consist of comminuted bone fragments that may or may not be driven into the brain.

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6
Q

With a high-velocity blunt injury you need to be worried about what?

A
  • Basilar skull fractures are common with high-velocity blunt injuries.
    • These fractures may extend through the cribiform plate or petrous bone and result in CSF leaks (otorrhea or rhinorrhea) that may lead to meningitis
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7
Q

What is a “growing fracture”

A

• Growing fractures of infancy (0-18 months of age) result from dural tears and herniation of the arachnoid into the fracture site. CSF pulsations then cause bone loss over months, often requiring surgical correction.

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8
Q

What is an epidural hematoma?

A
  • Intracranial, extradural arterial bleeding
    • Trauma in distribution of middle meningeal artery
    • Classically - impact, lucid interval, progressive obtundation and coma
    • Treatment is surgical removal of the mass lesion
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9
Q

What is a subdural hematoma?

A
  • Cause - translational acceleration from high velocity mechanisms
    • Hemorrhage- rupture of the bridging veins that connect the cortical surface of the brain with the sagittal sinus.
    • often associated with underlying cerebral contusions
    • Treatment includes prompt surgical removal of the blood clot, control of the intracranial pressure, and restoration of adequate cerebral blood flow.
    • Mortality - 40-60%
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10
Q

Where might you likely find cerebral contusions?

A
  • Superficial hemorrhagic areas in brain
    • Locations - brain surfaces in contact with particular bony areas:
    • rough bony surface of the anterior cranial fossa (frontal lobe)
    • sharp edge of the greater wing of the sphenoid (temporal lobe).
    • Hemorrhage into areas of damaged brain results in mass effect and herniation with secondary brain injury.
    • Treatment involves medical management to prevent brain swelling and occasional surgical evacuation of large hematomas.
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11
Q

What causes Diffuse axonal injury?

A
  • AKA - DAI
    • High velocity rotational accel/decel
    • Retraction balls on histology from shearing of axons
    • Clinical unconsciousness from injury but no anatomical correlation on CT
    • MRI - punctuate hemorrhages in large white matter tracts such as corpus callosum
    • Also near the grey-white junction where shearing occurs because of different densities of grey vs. white matter
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12
Q

Describe the extent of injury involved in DAI

A
  • Diffuse axonal injury
    • Injury exists along a spectrum
    • (one end) primary mechanical breaking of the axonal cytoskeleton,
    • to transport interruption,
    • swelling and proteolysis, through secondary physiological changes.
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13
Q

How can the spectrum of injury in DAI be clinically manifested?

A
  • Depending on the severity and extent of injury, these changes can manifest:
    • acutely as immediate loss of consciousness or confusion
    • persist as coma and/or cognitive dysfunction.
    • TBI may induce long-term neurodegenerative processes, such as insidiously progressive axonal pathology.
    • axonal degeneration has been found to continue even years after injury in humans, and appears to play a role in the development of Alzheimer’s disease-like pathological changes.
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14
Q

How can injury to the CNS be divided?

A
  • Into two temporal parts.
    • Initial injury and secondary injury
    • Initial injury is irreversible b/c of poor regen in CNS
    • Secondary injury comes from inadequate resuscitation/responses to the initial injury
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15
Q

What body responses to the initial CNS injury might cause a secondary injury?

A
  • Mechanisms include hypoxia, altered cerebral blood flow (dysautoregulation), and release of free radical mediators.
    • The free radical mediators break down the blood brain barrier and result in interstitial (vasogenic) edema.
    • The combination of events results in brain swelling, elevated intracranial pressure (ICP), further hypoxia, dysautoregulation, and herniation
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16
Q

What does the monroe-kellie doctrine describe?

A
  • Using the fact that the brain is in a rigid container to use hydrodynamic principles of pressure and volume to model secondary injury
    • All the volume contributers are part of a pie-chart, and they must equal the volume of the cranial cavity
    • If one contributer grows the others must make room (displacement of venous blood or CSF out the intracranial compartment)
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17
Q

Fluid is incompressible and the cranium is a fixed container. What is the consequence of this in terms of ICP?

A

• Once a certain volume is reached, the pressure grows exponentially

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18
Q

Why are you worried about ischemia or lack of blood blow with increased intracranial pressure?

A
  • Fast pressure increase will result in an ICP which approaches mean arterial pressure.
    • The net result is reduction and ultimately cessation of cerebral blood flow.
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19
Q

What causes herniation syndromes?

A

• Because the ICP is somewhat variable between the intracranial compartments
○ (the two sides of the falx, the supratentorial versus infratentorial compartment, and the compartment above and below foramen magnum),
• a forcible displacement of brain tissue across the falx, tentorium, or foramen magnum can result.
•

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20
Q

What might cause the mass effect that leads to brain herniation?

A
  • Trauma
    • Ischemia
    • Neoplasm
    • Infection
    • hydrocephalus
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21
Q

What are the 4 herniation syndromes you should be familiar with?

A
  1. Subfalcine herniation
    1. Central herniation
    2. Uncal herniation
    3. Tonsillar herniation
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22
Q

What is up with a subfalcine herniation?

A
  • cingulate gyrus is pushed away from the expanding mass and herniates beneath the falx cerebri.
    • In the process, the anterior cerebral artery is often kinked
    • stroke in the distribution of this vessel is not uncommon.
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23
Q

What’s up with uncal herniation?

A
  • Aka transtentorial
    • the uncus, a part of the medial temporal lobe, herniates across the tentorial edge, and downward into the posterior fossa.
    • It compresses the midbrain and its ipsilateral cerebral peduncle, usually producing an ipsilateral third nerve palsy and a contralateral hemiparesis or hemiplegia.
    • Rarely, uncal herniation can compress the opposite cerebral peduncle against the tentorial edge, resulting in a hemiparesis that is ipsilateral to the mass lesion and herniated uncus.
    • This phenomenon is referred to as a “Kernohan’s notch”.
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24
Q

What is “Kernohan’s notch”?

A

• Rarely, uncal herniation can compress the opposite cerebral peduncle against the tentorial edge, resulting in a hemiparesis that is ipsilateral to the mass lesion and herniated uncus.

25
Q

What causes a duret hemorrhage?

A
  • Uncal herniation can also produce a characteristic hemorrhage in the brainstem, a Duret hemorrhage,
    • produces devastating neurologic consequences, because of disruption of the ascending reticular activating system.
26
Q

What is impacted in a central herniation?

A

• Occurs when there is downward pressure centrally, and can result in bilateral uncal herniation.

27
Q

What’s up with tonsillar herniation?

A

• In tonsillar herniation the cerebellar tonsils herniate downward into the foramen magnum,
○ also referred to as “coning”.
• The medulla is compressed, and this can produce abnormal cardiac and respiratory responses,
○ Cushing’s reflex, which consists of bradycardia and hypertension in the setting of high intracranial pressure.
• Tonsillar herniation most commonly is encountered in the setting of a mass lesion in the posterior fossa.

28
Q

What procedure is bad news in the context of a herniation syndrome?

A

It is critical to recognize that a lumbar puncture in the setting of an intracranial mass lesion can precipitate a herniation syndrome, because of the differential pressures this creates between the cranial and spinal subarachnoid space

29
Q

Describe the pathophysiology of traumatic brain injury

A
  • In a word: excitotoxicity
    • Compounded by many factors
    • Inciting event is the TBI and mechanical forces cause massive neuronal depolarization, with massive neurotransmitter release
    • Pathologically high levels of glutamate complicate matters by increasing Ca++ influx into cells
    • Too much calcium leads to intracellular damage by activating a number of enzymes, including phospholipases, endonucleases, and proteases such as calpain.
    • Further, they go on to damage components of the blood-brain barrier, resulting in increased permeability which gives rise to additional brain swelling—this is known as vasogenic edema
    • Lastly, there is the potassium problem
    • So much potassium in synapse reverses the glutamate transporter in the glia and makes excitotoxicity problem even worse
    • Astrocytic swelling as a result causes cytotoxic edema, which will also shut off capillaries (astrocytic processes)
30
Q

How are capillaries shut off in cytotoxic edema?

A

• Astrocytic swelling as a result causes cytotoxic edema, which will also shut off capillaries (astrocytic processes)

31
Q

How is intracellular calcium linked to neuronal damage in TBI?

A
  • Pathologically high levels of glutamate complicate matters by increasing Ca++ influx into cells
    • Too much calcium leads to intracellular damage by activating a number of enzymes, including phospholipases, endonucleases, and proteases such as calpain.
    • Further, they go on to damage components of the blood-brain barrier, resulting in increased permeability which gives rise to additional brain swelling—this is known as vasogenic edema
32
Q

What is the potassium problem in TBI?

A

So much potassium in synapse reverses the glutamate transporter in the glia and makes excitotoxicity problem even worse
*this transporter is na-dependent symporter of glutamate. needs high extracellular sodium and high intracellular potassium to work
• Astrocytic swelling as a result causes cytotoxic edema, which will also shut off capillaries (astrocytic processes)

33
Q

You clinically manage elevated ICP via TBI how?

A
  • Treatment is based on minimizing ICP and maximizing oxygen and metabolite delivery.
    • accomplished by manipulating the three intracranial compartments:
    • 1) the intravascular space
    • 2) the brain parenchyma, and
    • 3) the cerebrospinal fluid space.
34
Q

How do you manage the intravascular space in emergency measures for TBI unconscious patients?

A
  • controlled ventilation to a pCO2 of 35mmHg is advisable
    • pCO2 can be reduced transiently to 25mmHg with a resultant decrease in blood volume (because of vasoconstriction) and subsequent lowering of ICP.
    • Elevation of the head prevents venous congestion.
    • Intravascular osmotic diuretics (e.g. mannitol, 1gm.kg body weight) develop osmotic and oncotic gradients across both the intact and injured blood brain barrier to reduce interstitial brain edema.
35
Q

What are emergency measures for all unconscious patients?

A
  • ABCs of basic life support to maintain oxygen delivery and adequate blood pressure.
    • Early endotracheal intubation is mandatory in unconscious patients to protect the airway and prevent hypoxia.
    • Then manage the three areas (intravascular space, brain parenchyma and CSF space)
36
Q

How do you manage the brain parenchyma in TBI unconscious patients?

A

• drug induced coma with barbiturates decreases metabolic demand and scavenges free radicals.

37
Q

What is the procedure for managing the CSF space?

A
  • Surgical and more invasive

* Ventricular catheters are used to drain the CSF spaces and treat any obstructive hydrocephalus that may be present.

38
Q

You need to know GCS very well. What are the three categories?

A
  • Eye opening (E)
    • Best motor response (M)
    • Verbal Response (V)
39
Q

What are the verbal response values in the GCS table?

A
  • Oriented - 5
    • Confused - 4
    • Inappropriate words - 3
    • Incomprehensible sounds - 2
    • None - 1
40
Q

What are the best motor response values in the GCS table?

A
  • Obeys commands - 6
    • Localizes pain - 5
    • Flexion - 4
    • Abnormal flexion (decorticate) - 3
    • Extension (decerebrate) - 2
    • None - 1
41
Q

What are the Eye Opening values in the GCS table?

A
  • Spontaneous - 4
    • To speech - 3
    • To pain - 2
    • None - 1
42
Q

What is the worst risk of an operable intracranial mass lesion in a GCS score of 15?

A
  • If they have a skull fracture and PTA

* 1/29

43
Q

What are the risks involved with a GCS score of 3-8?

A
  • No fracture - 1/27

* Fracture - 1/4

44
Q

What are the risks involved with a GCS score of 9-14?

A
  • No fracture - 1/180

* Fracture - 1/5

45
Q

What is a concussion?

A
  • A concussion, or mild traumatic brain injury, is an alteration in mental status caused by biomechanical forces that may or may not cause loss of consciousness.
    • The hallmarks of concussion are confusion and amnesia.
46
Q

What are common concussion symptoms?

A
  • The most common symptoms of concussion include headache,
    • dizziness,
    • poor attention,
    • inability to concentrate,
    • memory problems,
    • fatigue,
    • irritability,
    • depressed mood,
    • intolerance of bright light or loud noise, and
    • sleep disturbance
47
Q

LOC is required for concussion, yes?

A
  • No, absolutely not
    • There is usually a confusional episode and often amnesia
    • But LOC is not a necessary component of concussion
48
Q

What is the colorado comission grading scale for concussions?

A
  • Grade 1 - confusion without amnesia nor LOC
    • Grade 2 - confusion and amnesia
    • Grade 3 - LOC
49
Q

What is second impact syndrome?

A
  • rare but usually fatal consequence of a second concussion while still suffering the effects of an earlier one.
    • Usually in young adults in sports or recreational activities.
    • 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.
50
Q

What does management of concussion look like?

A
  • Careful observation by either responsible adult or by medical pro for 24 hours
    • Unless there is prolonged amnesia or LOC, waking up often is not needed
    • Definitely do the full neuro exam for a baseline in the recovery process
    • Advise a second formal neurophyschological consultation before being cleared to return to high risk activities
51
Q

What is the pharmacological treatment for concussions?

A
  • Acetaminophen should be offered for headaches and body pain (whiplash neck pain)
    • Considered safe in acute phase of injury
52
Q

What is considered a mild, moderate and severe TBI?

A
  • Based off of GCS
    • Mild - 15-13
    • Moderate - 12-9
    • Severe - 8-3
53
Q

An athlete that is rendered unconscious for more than 5 minutes is considered what?

A
  • A neurosurgical emergency

* Call that consult and get some images

54
Q

What lobes of the brain are most affected by head trauma?

A

• Frontal and temporal regardless of the direction of the force

55
Q

Linear (translational) forces can cause what?

A
  • Skull fractures and contrecoup contusions

* Skull fracture on impact side, contusions on contralateral side

56
Q

Which is better for detecting brain lesions, MRI or CT?

A
  • MRI is far better. CT is far faster

* huh

57
Q

Rotational injuries tend to be worse…why?

A

• Rotational injuries lead to diffuse shearing of small vessels
*results in diffuse axonal injury

58
Q

What is meant by SAC?

A 
• Standardized assessment of concussion
	• Standardized mental status examination
	• Composit total score (30pt scale)
	• Neurocognitive domains
		○ Orientation, concentration, immediate/delayed memory
	• Neurologic screening
	• Exertion/provocative maneuvers
	• Alternate forms A,B,C
	• 5-7 minutes to administer

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