Anatomy and Physiology XIV

Question 1

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

Answer 1

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

Question 2

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

Answer 2

Superior saggital sinus (p.425)

Question 3

What channel connects the lateral ventricles to the third ventricle?

Answer 3

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

Question 4

What channel connects the third ventricle to the fourth ventricle?

Answer 4

The cerebral aqueduct of Sylvius (p.426)

Question 5

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

Answer 5

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

Question 6

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

Answer 6

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

Question 7

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

Answer 7

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

Question 8

Where is CSF made?

Answer 8

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

Question 9

Where is CSF reabsorbed?

Answer 9

By arachnoid granulations (p.426)

Question 10

Where does CSF drain?

Answer 10

Into the dural venous sinuses (p.426)

Question 11

What causes communicating hydrocephalus?

Answer 11

Decreased CSF absorption by arachnoid granulations (p.426)

Question 12

What signs and symptoms may be caused by communicating hydrocephalus?

Answer 12

Increased ICP, papilledema, herniation (p.426)

Question 13

Name three types of communicating, non obstructive hydrocephalus?

Answer 13

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

Question 14

What distinguishes communicating from non-communicating hydrocephalus?

Answer 14

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

Question 15

Name one potential cause of communicating hydrocephalus.

Answer 15

Arachnoid scarring post meningitis (p.426)

Question 16

What clinical pathology leads to normal pressure hydrocephalus?

Answer 16

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

Question 17

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

Answer 17

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

Question 18

What CT findings are consistent with normal pressure hydrocephalus?

Answer 18

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

Question 19

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

Answer 19

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

Question 20

Name three potential causes of hydrocephalus ex vacuo.

Answer 20

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

Question 21

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

Answer 21

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

Question 22

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

Answer 22

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

Question 23

What causes noncommunicating hydrocephalus?

Answer 23

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

Question 24

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

Answer 24

Stenosis of the aqueduct of Sylvius (p.426)

Question 25

What is the pathophysiology of vertebral disk herniation?

Answer 25

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