Week 8 - Intracranial Regulation & ICP Flashcards

1
Q

define cranium

A
  • the collective bone structure that encloses the brain

- AKA the skull

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2
Q

what does intracranial mean?

A
  • refers to all components inside the skull

- the brain, circulatory system, and dura mater

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3
Q

define intracranial regulation

A
  • mechanisms of conditions that impact intracranial processing & function
  • focuses on conditions that specifically affect the contents of the cranium
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4
Q

describe the scope of ICR

A

ranges from

  • normal & optimal function to
  • impairment
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5
Q

what does brain function depend on

A
  • a constant supply of blood delivering O2 and nutrients
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6
Q

what specific nutrient provides fuel for the brain?

A
  • carbs = bg important
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7
Q

what 2 organs does the brain rely on for perfusion

A
  • lungs

- heart

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8
Q

what is the function of the skull

A
  • composed of multiple bones that acts as a rigid, noncompliant protective covering for the brain
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9
Q

what 3 components are found within the skull? what are their %?

A
  • brain tissue (80%)
  • blood (10%)
  • CSF (10%)
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10
Q

what is intracranial pressure

A
  • the sum of the pressure exerted by the 3 components in the skull (tissue, blood, and CSF)
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11
Q

what is the monra-kelli doctrine

A
  • the total volume inside the skull cannot change, since the skull is noncompliant (it does not stretch)
  • therefore, a change in one compartment must be compensated by a decrease in another component
    ex. if blood increased, then CSF will have to decrease to make room, etc.
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12
Q

what are the meninges

A
  • a tough protective membrane made of 3 layers that surrounds the brain and spinal cord
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13
Q

what are the 3 layers of the meninges

A
  • duramater (outer layer)
  • arachnoid mater
  • pia mater
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14
Q

what is the space between the arachnoid layer & pia mater called? what does it contain?

A
  • subarachnoid layer

- contains CSF

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15
Q

what is the dura mater attached to?

A
  • the skull
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16
Q

what is the CSF? what is its function? (2)

A
  • cerebrospinal fluid

- cushions & supports the brain & other structures (such as the spinal cord) of the CNS & provides nutrients

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17
Q

describe how the Monro-Kelli compensation changes over time; what does this result in?

A
  • at first, small increases in the volume can be compensated and ICP remains the same (or close to)
  • but as the intracranial volume continues to increase, the compensatory mechanisms fail
  • results in increased ICP
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18
Q

what is normal ICP? what is considered intracranial HTN?

A
  • normal <15 mmHg

- >20 HTN

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19
Q

what can cause increased ICP? (6)

A
  • brain hemorrhage
  • trauma
  • edema
  • infection
  • tumours
  • excessive amt of CSF
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20
Q

what can increased ICP cause? (3)

A
  • obstruct cerebral blood flow (can compress blood vessels)
  • destroy brain cells
  • displace brain tissue (herniation)
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21
Q

describe how the brain can compensate for increased ICP

A
  • can move CSF to another location

- vasconstriction of cerebral arteries to decrease blood flow into the brain

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22
Q

what is the fnxn of the brainstem? what is the 3 parts?

A

controls life-sustaining processes

  • midbrain
  • pons
  • medulla
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23
Q

what is the function of the medulla (3)

A

plays important role in vital functions:

  • CVS
  • resp
  • reflexive actions
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24
Q

what reflexive actions is the medulla responsible for (4)

A
  • swallowing
  • coughing
  • sneezing
  • vomiting
25
Q

what causes the early signs of increased ICP

A
  • pressure on the brainstem & meninges

- hypoxia to sensitive cortical neurons

26
Q

list the 4 early signs of increased ICP

A
  • decreased LOC
  • severe headache
  • vomitting
  • papilledema
27
Q

what causes decreased LOC during increased ICP

A
  • pressure on the reticular activating system

- hypoxia of cortical neurons which

28
Q

what is the RAS? where is it found? what does it do?

A
  • network of neurons found in the brainstem

- responsible for arousal, awareness, and sleep-wake cycle

29
Q

what does pressure on the RAS cause

A
  • decreased responsiveness & arousal
30
Q

what does hypoxia of the cortical neurons cause

A
  • altered cognition
31
Q

how does increased ICP cause a headache (2)

A
  • due to stretch on the dura mater –> pain receptors

- stretch on blood vessels

32
Q

how does increased ICP cause vomitting?

A
  • due to pressure on the emetic center (in the medulla)
33
Q

what does vomitting do to increased ICP look like? (3)

A
  • may be projectile
  • rapid
  • w/o nausea
34
Q

what is papilledema

A
  • swelling of the optic nerve
35
Q

how does increased ICP cause papilledema

A
  • compresses the optic nerve, and the retinal veins & arteries
36
Q

what is Cushing’s reflex/triad? what does it include?

A
  • set of signs indicative of increased ICP
    1. increased systolic BP (and widened pulse pressure)
    2. decreased HR
    3. decreased RR
37
Q

describe how increased ICP causes increased systemic BP

A
  • as ICP rises, we get ischemia to the brain
  • this ischemia and lack of O2 is detected by the CVS control center in the medulla
  • this triggers efferent signals from the vasomotor area causing systemic vasoconstriction
    = increased bp to try and perfuse the brain
38
Q

describe how increased ICP causes decreased HR

A
  • the rise in BP initiates a baroreceptor reflex which lowers the HR ( only effect the HR, not blood vessel constriction)
39
Q

describe how increased ICP causes decreased RR (3)

A

unknown but 3 proposed mechanisms:

  1. P on the resp centre in the medulla causes impaired function & a decline in RR or cheyne-stokes respiration
  2. increased sensitivity to PCO2
  3. accelerated systemic circulation
40
Q

what are cheynes-stokes respiration

A
  • periods of apnea

- followed by a period of rapid breathing with an increasing then decreased tidal volume

41
Q

how can increased ICP cause herniation

A
  • by causing displacement on the brain within the cranium
42
Q

what are 4 types of brain herniations

A
  • cingulate
  • central
  • uncal
  • cerebellar
43
Q

what does the dura mater form? give 2 examples

A
  • the meningeal folds
    1. falx cerebri
    2. tentorium
44
Q

what is the falx cerebri

A
  • fold that goes down into the longitudinal fissure

- separates the two hemispheres of the brain

45
Q

what is the tentorium

A
  • fold that separates the cerebrum from the cerebellum
46
Q

what is the foramen magnum

A

-opening at the base of the skull thru which the spinal cord exits

47
Q

what is an uncal herniation

A
  • when the temporal lobe is pushed under the tentorium cerebelli
48
Q

what does an uncal herniation result in?

A
  • compresses the oculomotor nerve (in the brainstem) and posterior artery
    = ipsilateral pupil dilation & ischemia
49
Q

what does ipsilateral mean

A
  • occuring on the same side
50
Q

what is the posterior cerebral artery

A
  • one of a pair of arteries that supplies blood to the occipital lobe
51
Q

what is a central herniation

A
  • parts of both temporal lobes herniate thru the tenotiral notch
52
Q

what does a central herniation cause

A
  • downward pressure on the brainstem & brainstem dysfunction
53
Q

what is a cingulate herniation

A
  • when the innermost part of the frontal lobe (cigulate gyrus) gets squeezed under the falx cerebri to the opposite hemisphere
54
Q

what does a cingulate herniation often result in

A
  • coma / unconscious
55
Q

what is the cingulate gyrus responsible for

A
  • processing emotions & behavior regulation
56
Q

what is a cerebellar herniation

A
  • part of the cerebellum pushes thru the foramen magnum
57
Q

what does a cerebellar herniation often result in

A
  • impairment of brainstem function
58
Q

as pressure increases on the brain stem due to herniation, what occurs

A
  • motor strength & coordination becomes impaired
59
Q

what symptoms occur later due to increased P on the brainstem r/t herniation (5)

A
  • posturing
  • flaccidity
  • fixed & dilated pupils
  • unconciousness
  • resp arrest