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CCN > Neuro and Intracranial Dynamics > Flashcards

Neuro and Intracranial Dynamics Flashcards

1
Q

How does sensory info travel up the spinal cord?

A

Up through spinothalamic tracts through the brainstem and cerebellum to the cerebrum

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2
Q

How does motor info travel down the spinal cord?

A

Down through corticospinal tracts, through brainstem and cerebellum, down spinal cord to the effector organ

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3
Q

Where do the corticospinal tracts pass and what is the significance?

A

Cross at the level of the medulla, therefore movement on one side of the body is controlled by the other side of the brain.

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4
Q

What is decussation?

A

Cross over of descending motor tracts (corticospinal tracts) at the medulla

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5
Q

Which cranial nerves exit through the brainstem?

A

All except I and II

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6
Q

Do cranial nerves cross over?

A

No, so they are responsible for same side (ipsilateral) sensory and motor information

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7
Q

What is CN II responsible for and what occurs in deficits?

A

Vision

Deficits result in impaired visual fields

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8
Q

What is CN III responsible for and what occurs in deficits?

A

Raises eyelid, pupil constriction, eye movement

Deficits result in ptosis and pupil dilation

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9
Q

What is CN IX responsible for and what occurs in deficits?

A

Gag, swallowing, phonation

Deficits result in impaired gag and difficulty speaking

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10
Q

What is CN X responsible for and what occurs in deficits?

A

Swallowing

Deficits result in impaired swallowing and speech

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11
Q

What are the afferent / efferent portions of the pupil and corneal reflex?

A

Pupil:

CN II sees light
CN III constricts pupil

Corneal:

CN V detects stimulus
CN VII causes facial twitch

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12
Q

What is the weakest point of the skull and why is it vulnerable?

A

Pterion –> Junction of the skull bones

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13
Q

What are the divisions of the skull base?

A

Anterior, middle, posterior fossa

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14
Q

What are the 3 main areas of the brain?

A

1) Cerebrum
2) Cerebellum
3) Brainstem

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15
Q

What are elements of the cerebrum?

A

2 central hemispheres composed of pairs of:

1) Frontal lobe
2) Parietal lobe
3) Temporal lobe
4) Occipital lobe

Central hemispheres communicate through corpus collosum

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16
Q

What is the frontal lobe responsible for?

A

Contains motor cortex
High level cognitive functioning, concentration, judgment, memory, emotion, personality.

Contains Broca’s area responsible for motor speech

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17
Q

What happens with frontal lobe deficits?

A

Contralateral motor impairment, behaviour and personality changes, impaired speech

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18
Q

What is the parietal lobe responsible for?

A

Contains sensory cortex

Interpret sensations, proprioception

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19
Q

What happens with parietal lobe deficits?

A

Sensation deficits, left and right confusion, neglect syndromes

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20
Q

What is the temporal lobe responsible for?

A

Auditory lobe
Integration of auditory and visual areas, contains Wernike’s area responsible for understanding of speech.
Visual, auditory, olfactory perception, learning, memory

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21
Q

What happens with temporal lobe deficits?

A

Receptive aphasia if Wernike’s area is damaged

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22
Q

What is the occipital lobe responsible for?

A

Visual perception, visual reflexes, smooth eye movements

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23
Q

What is the cerebellum?

A

Located in posterior fossa, controls fine movement and coordination of muscle groups, maintaining balance

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24
Q

What happens with cerebellar deficits?

A

Gait disturbances, ataxia, dysmetria (lack of coordination)

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25
Q

What is the reticular activating system (RAS)?

A

Group of nuclei throughout the brainstem, moderates wakefulness and consciousness.

Disturbances in RAS result in altered LOC, fibers fan out to all aspects of the cerebrum

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26
Q

What are the 3 main subdivisions of the brainstem?

A

1) Midbrain
2) Pons
3) Medulla

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27
Q

What is the midbrain responsible for?

A

Motor function, relay system between cerebral hemispheres, subcortical structures, cerebellum, and spinal cord

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28
Q

What is the pons responsible for?

A

Respiratory patterns, controlling rate

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29
Q

What is the medulla responsible for?

A

Extends through foramen magnum and becomes spinal cord.

Site of decussation, controls respiration, vomiting, hiccupping, vasomotor function affecting blood pressure

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30
Q

What happens with brain stem deficits?

A

Decreased LOC due to RAS
Pupil changes due to CN III sitting on top of midbrain
Motor, sensory impairments
Vital signs changes including RR

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31
Q

What are the 3 layers of the meninges?

A

1) Dura mater
2) Arachnoid membrane
3) Pia mater

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32
Q

What is the dura mater?

A

Outer layer of meninges lining interior of the skull. Subdual space is potential space between dura mater and skull.

Folds in the dura mater forms the falx and tentorium.

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33
Q

What is the arachnoid membrane?

A

Middle layer of meninges with web-like structure allowing passage of blood via cerebral arteries and veins.

CSF flows in subarachnoid space between arachnoid and pia mater.

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34
Q

Which space does CSF flow through?

A

CSF flows in subarachnoid space between arachnoid and pia mater.

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35
Q

What absorbs CSF?

A

Arachnoid villi

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36
Q

What is the pia mater?

A

Inner layer of meninges, vascular membrane attached to the brain surface.

Gets blood from internal carotid and vertebral arteries.

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37
Q

What does the brain ventricular system consist of?

A

2 lateral ventricles, the third ventricle, and fourth ventricle

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38
Q

Where is CSF produced?

A

At the choroid plexus lining the two lateral ventricles, third and forth ventricle

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39
Q

What is the function of CSF?

A

Fills ventricles and subarachnoid space, acts as shock absorber and buffer for increased ICP.

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40
Q

What is the flow of CSF through the brain?

A
  • -> Lateral ventricles
  • -> Foramen of Monro
  • -> 3rd Ventricle
  • -> Cerebral aqueduct
  • -> 4th ventricle

–> Foramen of Magendie down around spinal cord OR Foramen of Luschka up around cerebral hemispheres

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41
Q

Where does CSF flow out of the brain?

A

Gets absorbed via arachnoid villi, reabsorbed through the superior sagittal sinus back into venous circulation via jugular veins

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42
Q

How is the brain supplied with oxygen?

A

1) 2 internal carotid arteries

2) 2 vertebral arteries

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43
Q

Explain anterior and posterior circulation in the brain

A

Anterior circulation refers to common carotids and their branches, with the internal carotid arteries supplying 80% of the cerebrum

Posterior circulation refers to the vertebral arteries and their branches, which supply blood to the brainstem, cerebellum and occipital lobes

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44
Q

Where do anterior and posterior circulation connect?

A

At the circle of Willis

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45
Q

What is the only venous drainage of the brain?

A

Jugular veins

46
Q

What is ICP?

A

Pressure within the cranium

47
Q

What is the normal ICP?

A

0-15 mmHg

48
Q

What is the threshold for high ICP and when should we treat it?

A

High ICP is > 20mmHg for > 5mins

Brain Trauma Foundation Guidelines: Treat ICP > 22mmHg

49
Q

How is ICP measured?

A

1) External Ventricular Device

2) Intraparenchymal device

50
Q

What is the cornerstone of ICP assessment?

A

LOC

51
Q

What are early signs of increased ICP?

A 
Altered LOC 
Headache
N/V
Motor dysfunction 
Changes in speech 
Visual disturbances
52
Q

What are late signs of increased ICP?

A

Profound decrease in LOC
Abnormal motor responses
Changes in VS and Resp pattern
Pupil changes

53
Q

At what ICP and CCP do we notify MD if no orders?

A

ICP > 20mmHg for 5 mins

CCP < 60 for 5 mins

54
Q

What is the Monro-Kellie hypothesis?

A

ICP = V (Brain) + V (CSF) + V (Blood)

55
Q

How does blood affect ICP?

A

10% of overall volume
Most easily influenced in the clinical setting

Affected by jugular venous outflow, autoregulation, CO2, CPP

56
Q

How does brain affect ICP?

A

80% of overall volume

57
Q

How does CSF affect ICP?

A

10% of overall volume

Primary buffer for ICP, most rapidly displaced by volume increases of brain or blood

58
Q

What is the body’s primary compensatory mechanism for increased ICP?

A

Shunting of CSF into larger cisterns and/or to spinal cord

59
Q

What are the compensatory mechanisms for increased ICP?

A

1) SHUNTING CSF
2) Increased venous outflow
3) Compression of brain tissue

60
Q

Why does location of lesions matter in ICP compensation?

A

Lesions altering patency of CSF pathways lead to rapid deterioration as cannot compensate

61
Q

What is intracranial compliance?

A

Ability of brain to tolerate increases in intracranial volume without sustaining increase in pressure

62
Q

What clinical assessments show intracranial compliance?

A

Higher the ICP, worse compliance

ICP response to stimulation is high, worse compliance

If P2 of ICP waveform is higher than P1, poor compliance. Higher the amplitude (pulse pressure) of ICP waveform, worse compliance

63
Q

What is autoregulation and how does it work in the brain?

A

Ability of organ to maintain constant blood flow within a broad range, despite changes in arterial perfusion pressure

Cerebral autoregulation –> cerebral vessels dilate or constrict to preserve adequate blood flow

As SBP increases, cerebral vessels vasoconstrict
As SBP decreases, cerebral vessels vasodilate

64
Q

What can cause cerebral autoregulation to fail?

A

Severely increased ICP, extreme hypo/hypertension, trauma, cerebral ischemia, extreme elevations in PaCO2

65
Q

What is hydrocephalus and what are the types?

A

Imbalance between how much CSF is being produced and absorbed or how it flows through the ventricular system.

1) Non-communicating (obstructive) hydro
2) Communicating (non-obstructive) hydro

66
Q

What is non-communicating hydrocephalus?

A

CSF does not flow properly because of obstruction, can be caused by tumor, congenital defect, or inflammatory process

67
Q

What is communicating hydrocephalus?

A

CSF flows through proper tracts but is not reabsorbed normally by the arachnoid villi due to damage to the villi

Can occur from TBI, subarachnoid hemorrhage (blood plugs up arachnoid villi) or exudates from meningitis. Rarely can be over-production of CSF from choroid plexus

68
Q

What are physiologic factors that can increase blood volume in the brain?

A
  • Increased cerebral metabolic demand, e.g. pain, seizures, fever
  • Obstruction of venous flow
  • Increased intra-abdominal pressure
  • Poor pt positioning
  • PaCO2 due to cerebral vasodilation
69
Q

How do we position the pt to optimize blood flow to and from the brain?

A

Head of bed elevated at least to 30%, in midline position

70
Q

What are the two potential spaces and one actual space in the meninges?

A

1) Epidural space (above the dura, below the skull)
2) Subdural space (below the dura, above the arachnoid layer)

Actual space: 
Subarachnoid space (below arachnoid layer, above pia mater) where CSF flows freely
71
Q

What is epidural hematoma?

A

Bleeding into potential space between skull and dura mater. Caused by direct blow to head, often around the pterion lacerating middle meningeal artery.

Arterial in origin. Large mass rapidly increases ICP

72
Q

What is the classic clinical presentation of epidural hematoma?

A

Momentary unconsciousness followed by lucid period of minutes to hours, then rapid deterioration (Walk talk die)

73
Q

What is subdural hematoma?

A

Bleeding between the dura mater and arachnoid layer. Caused by tearing of bridging veins.

Venous in origin, more common than EDH.
Cerebral atrophy in older pts gives more free space to fill up before symptoms present.

74
Q

What is subarachnoid hemorrhage?

A

Bleeding into the subarachnoid space, caused by TBI, AVM, or cerebral aneurysm (aSAH)

75
Q

What is aneurysmal subarachnoid hemorrhage?

A

Rupture of cerebral aneurysm usually occurring at base of the brain and arising from Circle of Willis at bifurcation points.

Release of arterial blood at high pressure into subarachnoid space.

76
Q

What are signs + symptoms of aSAH?

A

Sudden onset severe thunderclap headache, GCS can range 3-15 with n/v, nuchal rigidity, ipsilateral or bilateral dilated pupils, motor defects

77
Q

What are the main complications of aSAH?

A
  • Rebleeding (high risk in 24hrs), must manage until aneurysm is secured
  • Acute hydrocephalus (blood blocks arachnoid villi)
  • ECG changes (massive catecholamine response shows QT prolongation, T wave changes)
  • Hyponatremia
  • Delayed cerebral ischemia (may be caused by vasospasm, focal neurologic impairment or decrease > 2 pts of GCS lasting at least 1 hr)

-VASOSPASM (delayed arterial narrowing, similar to stroke)

78
Q

What is post aSAH vasospasm?

A

Delayed arterial narrowing 3-21 days after initial aneurysm rupture, peaks at 7-10. Caused by irritation of blood around arterial walls.

Prevention supported through normovolemia, normothermia, oxygenation. Nimodipine (Ca+ channel blocker) can reduce incidence but watch for systemic hypotension

79
Q

What is intracerebral hemorrhage?

A

Bleeding into the brain tissue, commonly by hypertension or from trauma

80
Q

What are the two main consequences of increased ICP?

A

1) Cerebral herniation

2) Cerebral hypoperfusion

81
Q

Where is the Falx Cerebri?

A

Dural fold located between left and right hemispheres at the top of the cerebrum

82
Q

Where is the tentorium cerebri?

A

Dural fold separating cerebrum from the cerebellum and runs along base of the temporal lobe. Opening in the center called temtorium hiatus allowing cerebrum to connect to the rest of CNS

83
Q

What happens if pressure is put on RAS?

A

RAS originates in brainstem but fans out to other parts of cerebral hemispheres. Pressure –> altered LOC

84
Q

What happens if pressure is put on the descending motor pathways?

A

They travel through the tentorium hiatus and cross at the medulla. Pressure causes contralateral limb weakness

85
Q

What happens if pressure is put on the CN III (occulomotor)?

A

Exits brainstem at the top of the midbrain. Pressure –> pupil dilation

86
Q

What happens if you put pressure on the cerebral vasculature?

A

Circle of Willis sits around tentorium hiatus. Pressure –> Occlusion of blood flow to the brain

87
Q

What happens if you put pressure on the brainstem?

A

Pons controls resp rate and medulla controls resp, cardiac, BP centers so changes in VS

88
Q

What is mass effect?

A

Cerebral edema or lesions occupying space within cranial vault eventually cause shift or herniation of brain tissue.

89
Q

What are the 4 types of herniation?

A

1) Subfalcine
2) Central
3) Uncal
4) Cerebellar tonsillar herniation / Coning

90
Q

What happens in subfalcine herniation?

A

Lesion in one hemisphere causes pressure medially displacing brain under the falx cerebri to the opposite side.

91
Q

What happens in central herniation?

A

Lesion produces downward displacement of cerebral hemispheres through the tentorium hiatus. Often result from global edema or mass lesions in frontal/parietal region.

92
Q

What are clinical signs of central herniation?

A

Initially bilateral small reactive pupils in early stage (RAS), then end point fixed dilated pupils (CN III).

Profound decrease LOC. Motor deficits. Abnormal resp patterns

93
Q

What is uncal herniation?

A

Displacement of medial temporal lobe (uncus) into the tentorium hiatus, compressing third cranial nerve and surrounding structures

94
Q

What are clinical signs of uncal herniation?

A

Ipsilateral pupil dilation, first sluggish then non-reactive. Altered LOC, contralateral hemiparesis, abnormal resps

95
Q

What is cerebellar tonsillar herniation (Coning)?

A

Downward displacement of cerebellar tonsils and medulla through the foramen magnum

Rapidly fatal

96
Q

What are clinical signs of cerebellar tonsillar herniation?

A

Bilaterally fixed and dilated pupils, GCS 3 deterioration, abnormal motor responses, cushing’s triad

97
Q

What is CPP? What is normal?

A

Net pressure of blood flow into the brain.

CPP = MAP - ICP

Normal CPP = 70-100 mm Hg
Brain trauma foundation recommendation for target CPP value is 60-70mmHg.

98
Q

If CPP is low, what to treat first? ICP or MAP?

A

Treat high ICP first, MAP will follow as it is a compensatory mechanism for low CPP in the first place

99
Q

Why are neuro pts at risk for fluid and electrolyte abnormalities?

A

Can develop diabetes insipidus, SIADH, Cerebral salt wasting

Avoid using D5W as maintenance infusion as glucose can cross BBB and draw fluid into brain increasing ICP

100
Q

Why do neuro pts need nutrition?

A

Due to increased ICP, pts are hypermetabolic and hypercatabolic

101
Q

What are MAP targets for neuro pts with high ICP?

A

Maintain SBP > 100mmHg or > 110 mmHg for younger and older pts to maintain adequate CPP

102
Q

How does mannitol work to treat increased ICP?

A

Draws fluid out of edematous cerebral tissue.

Caution: Diuresis may lead to hypovolemia and hypotension causing cerebral hypoperfusion.

Must monitor serum lytes and osmolarity

103
Q

How does hypertonic saline work to treat increased ICP?

A

3% saline decreases brain volume by drawing fluid out of edematous brain. Is also a plasma volume expander and improves blood pressure and ultimately CPP. Does not drop BP as much as mannitol.

104
Q

When should corticosteroids be used to treat increased ICP?

A

Only when cerebral edema is secondary to brain tumors.

NOT indicated for cerebral edema post TBI as it does NOT respond.

105
Q

How does decompressive craniectomy work to treat increased ICP?

A

Removal of a bone flap / part of the skull to increase potential volume of cranial cavity

106
Q

How to reduce CSF volume?

A

CSF can be drained via an ICP monitor inserted into the anterior horn of the lateral ventricles (External ventricular drain).

Pts with long term hydrocephalus may require a ventriculoperitoneal shunt.

107
Q

How to decrease blood volume in brain? Can we increase HOB to 45 degrees?

A

Proper pt positioning.

HOB to 45 degrees increases intrathoracic and intra-abdominal pressure which increases ICP. So NOT indicated

108
Q

Can we use hyperventilation to decrease ICP?

A

Should only be used for SHORT periods of time in emergency situations. Cannot be used routinely due to risk of cerebral hypoperfusion and ischemia.

PaCO2 should be maintained between 35-45

109
Q

Why is it important to maintain normothermia in ICP pts?

A

Fever significantly increases cerebral metabolic rate and causes increased blood flow to the brain.

110
Q

Why is it important to sedate / control pain in ICP pts?

A

Agitation and pain can increase cerebral metabolic rate and increase CBF, ICP. Propofol is a good med to use but must watch for hypotension

111
Q

What must we remember when giving NMBAs to ICP pts?

A

Once NMBAs are started, clinical neuro assessments cannot be completed

CCN (27 decks)

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