Anatomy and Physiology XIV Flashcards Preview

Neurology > Anatomy and Physiology XIV > Flashcards

Flashcards in Anatomy and Physiology XIV Deck (25)
1

From where do the dural venous sinuses brain blood/ CSF?

Blood from the cerebral veins; CSF from arachnoid granulations (p.425)

2

Where is the main dural venous sinus location of CSF return via arachnoid granulations.

Superior saggital sinus (p.425)

3

What channel connects the lateral ventricles to the third ventricle?

The right and left intraventricular foramina of Monro (p.426)

4

What channel connects the third ventricle to the fourth ventricle?

The cerebral aqueduct of Sylvius (p.426)

5

Name the two foramens of the fourth ventricle that connect to the subarachnoid space.

Foramen of Luschka and foramen of Magendie (p.426)

6

Describe the relative locations of the foramina of Luschka and the foramen of Magendie in relation to the fourth

Foramina of Luschka is lateral; Foramen of Magendie is medial (p.426)

7

To what do the Foramina of Luschka and the foramen of Magendie connect?

Connect the 4th ventricle to the subarachnoid space (p.426)

8

Where is CSF made?

By ependymal cells of the choroid plexus (p.426)

9

Where is CSF reabsorbed?

By arachnoid granulations (p.426)

10

Where does CSF drain?

Into the dural venous sinuses (p.426)

11

What causes communicating hydrocephalus?

Decreased CSF absorption by arachnoid granulations (p.426)

12

What signs and symptoms may be caused by communicating hydrocephalus?

Increased ICP, papilledema, herniation (p.426)

13

Name three types of communicating, non obstructive hydrocephalus?

Communicating hydrocephalus, normal pressure hydrocephalus, hydrocephalus ex vacuo (p.426)

14

What distinguishes communicating from non-communicating hydrocephalus?

Communicating is non-obstructive; noncommunicating is obstructive (p.426)

15

Name one potential cause of communicating hydrocephalus.

Arachnoid scarring post meningitis (p.426)

16

What clinical pathology leads to normal pressure hydrocephalus?

Increased subarachnoid space volume without increase in CSF pressure; expansion of ventricles distorts the fibers of the corona radiata (p.426)

17

What is the clinical triad of symptoms in normal pressyre hydrocephalus?

Urinary incontinence, ataxia, cognitive dysfunction (sometimes reversible); Wet, wobbly, wacky (p.426)

18

What CT findings are consistent with normal pressure hydrocephalus?

Lateral ventricle enlargement in absence of, or out of proportion to sulcal enlargement (which is a marker for brain atrophy) (p.426)

19

What signs and symptoms may be caused by hydrocephalus ex vacuo?

Appearance of increased CSF in the presence of atrophy. ICP is normal and wet, wobbly, wacky triad is not seen (p.426)

20

Name three potential causes of hydrocephalus ex vacuo.

Alzheimer's disease, advanced HIV, and Pick's disease (p.426)

21

What is the cause of the apparent CSF increase observed on imaging in hydrocephalus ex vacuo?

Decreased neural tissue due to neuronal atrophy (p.426)

22

What is the primary difference between normal pressure hydrocephalus and hydrocephalus ex vacuo?

Ventricular enlargement is out of proportion to atrophy in normal pressure hydrocephalus; increased CSF is accompanied by atrophy in hydrocephalus ex vacuo (p.426)

23

What causes noncommunicating hydrocephalus?

Structural blockage of CSF circulation within the ventricular system (p.426)

24

Give an exmaple of a condition which may cause noncommunicating hydrocephalus.

Stenosis of the aqueduct of Sylvius (p.426)

25

What is the pathophysiology of vertebral disk herniation?

Nucleus pulposus herniates through the anulus fibrosus (p.427)