Intracranial Pressure and Ventricles Flashcards

1
Q

What is the Monroe-Kellie doctrine?

A

If one part inside the skull gets bigger another has to get smaller.

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2
Q

What mechanisms are there to compensate for increased intracranial pressure?

A
  1. Movement of CSF into the spinal (thecal) sac
  2. Increased reuptake of CSF at the arachnoid villi
  3. Compression of veins and sinuses
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3
Q

What are the two types/causes of hydrocephalus?

A

Communicating (increased production of CSF or impaired absorption)

Non-communicating (blockage; most common)

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4
Q

What are the clinical features of increased ICP?

A
  1. Headache - worse in the morning, worse when stooping/bending over
  2. Altered mental status
  3. Nausea/vomiting
  4. Papilledema (result of long-standing elevated ICP)
  5. Diplopia
  6. Cushing’s triad: hypertension, bradycardia, irregular breathing
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5
Q

What are some pharmacologic and non-interventional ways to treat elevated ICP?

A

Reverse Trendelenburg position (elevate the head of the patient’s bed)

Hyperventilate the patient to vasoconstrict cerebral vessels

Mannitol to decrease edema via osmotic diuresis

Acetazolamide reduces CSF production via carbonic anhydrase inhibition

Sedation to reduce brain metabolism -> vasoconstriction

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6
Q

A 19 yo female presents with morning headaches and also complains of whooshing noise in her ears at night.

On exam, she has papilledema and difficulty abducting both eyes.

What is your Dx?

What would you expect opening pressure on LP be?

A

Idiopathic intracranial hypertension aka pseudo-tumor cerebri. LP opening pressure should be over 280mmHg in these patients.

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7
Q

What are the criteria for brain death?

A

No evidence of consciousness

No purposeful motor activity

No spontaneous respirations

Respiration requires the assistance of a ventilator

No brainstem reflexes

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8
Q

What is this position called (flexed upper extremity, extended and internally rotated lower extremity)? What does it indicate?

A

Flexor (decorticate) posturing.

Indicates severe damage at or above the midbrain level.

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9
Q

What is this position called (extended and internally rotated upper limb, extended lower limb)? What does it indicate?

A

Extensor (decerebrate) positioning.

Indicates damage extending below the midbrain.

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10
Q

What is normal pressure hydrocephalus and how does it present?

A

Enlarged ventricles but normal LP pressure.

Clinical triad: dementia, gait problems, urinary incontinence (wacky, wobbly, wet)

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11
Q

What type(s) of herniation can potentially compress CN III and the respiratory centers in the midbrain?

A

Uncal herniation, or tonsillar herniation.

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12
Q

Aneurysms of which cerebral artery can potentially cause ptosis, pupil dilation, and the eye(s) to be abducted and depressed? Which nerve is involved in this condition?

A

Aneurysms of the PCA can compress CN III

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13
Q

Name the cisterns

A
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14
Q

What are the layers of the choroid plexus?

A

endothelium of the choroid capillary (fenestrated)

pia matter (highly permeable)

ependymal cells (tight junctions)

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15
Q

What is the flow of CSF

A

Lateral ventricles

3rd venticle

Cerebral aqueduct

4th ventricle

Cisterna magna (via median and lateral apertures or central canal to lumbar cistern)

Subarachnoid space

Arachnoid villi

Superior sagittal sinus

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16
Q

What is ex-evacuo ventriculomegaly? What is the leading cause?

A

Compensatory (or ex-vacuo) ventriculomegaly is the secondary expansion of CSF-containing spaces due to the loss of brain parenchymal volume

Cerebral atrophy is a leading cause of ex-vacuo ventriculomegaly