Sinuses

Question 1

What is the cavernous sinus constituted by?

Answer 1

a plexus of veins.

Question 2

Nervous contents of the cavernous sinus?

Answer 2

CN III
CN IV
CN V1
——–
CN V2 (the only nerve of the cavernous sinus who does not exit the skull through the superior orbital fissure.) (rotundum)
———
The only one not attached to the lateral dural wall - the “only CN INSIDE the cavernous sinus” = CN VI

Question 3

What are the dural venous sinuses composed of?

Answer 3

They are venous channels intracranially between the two layers of dura mater - The endosteal layer and the meningeal layer.

Question 4

What differes venous sinuses in the brain from other veins in the body?

Answer 4

They run alone and not parallel to arteries. They are valveless, allowing for bidirectional flow into and from intracranial veins.

Question 5

What is the predominant exit vein for the intracranial sinuses?

Answer 5

The internal jugular veins.

Question 6

Are the draining territories of intracranial veins the same as the arterial territories of the major cerebral arteries?

Answer 6

No. They differ.

Question 7

Which are the major unpaired sinuses?

Answer 7

• Superior sagittal sinus
• Inferior sagittal sinus
• Straight sinus
• Occipital sinus
• Intercavernous sinus

Question 8

Which are the major paired sinuses of the brain?

Answer 8

• Transverse sinus
• Sigmoid sinus
• Super petrosal sinus
  *Inferior petrosal sinus
• Cavernous sinus
  *Sphenoparietal sinus
• Basilar venous plexus

Question 9

What special group is over represented with sinus trombosis?

Answer 9

Women on contraceptive pill.

Question 10

What are typical signs of sinus trombosis?

Answer 10

H/A, nausea, vomiting

Question 11

What is the pathology of sinus trombosis leading to cerebral swelling, venous hypertension, edema and hemorrhage?

Answer 11

SSS or the dominant transverse sinus can affect the arachnoid granulation absorption of CSF, leading to consequent swelling.

Question 12

What type of infection is a riskfactor for sinus trombosis?

Answer 12

Especially mastoid sinus infection - dural sinus occlusive disease.

Question 13

Name systemic illnesses that are riskfactors of sinus trombosis

Answer 13

• dehydration
• sepsis
• malignancy
• connective tissue disorders

Question 14

What is DSOD- dural sinus occlusive disease?

Answer 14

An infective form of dural sinus thrombosis, thromboflebitis, commonly seen in acute otomastoiditis.

Question 15

Typical signs of dural sinus occlusive disease (acute otomastoiditis

Answer 15

• severe H/A
• high fever
• Sixth nerve palsy - due to involvement of Dorellos canal
• altered conscious state

Question 16

Is it possible to exclude the diagnosis of dural sinus occlusive disease?

Answer 16

Yes. demonstration of normal flow in the dural venous sinus essentially excludes the diagnosis.

Question 17

In “normal” sinus trombosis, what are signs to look for in unenhanced CT?

Answer 17

• cord sign
• dense vein sign - same as cord sign but in cross-section (triangle)
• vasogenic edema
• unilateral or bilateral cortical or peripheral venous hemorrhage - including cashew nut sign.

Question 18

What is “cord sign” on unenhanced CT ?

Answer 18

Cordlike hyperattenuation within a dural venous sinus. Commonly seen in the transverse sinus.

Question 19

Why is cord sign more easy to see in the transverse sinus?

Answer 19

Because along the origin of the tentorium, it runs approximately in the axial plane such that it is visible on one image.

Question 20

What is a “false positive cord sign”?

Answer 20

In the setting of generalized cerebral edema, the brain is of reduced density rather than the sinus being hyperdense.

Question 21

Is it normal if “dense vein sign” is seen close to torcula herophili?

Answer 21

YES. blood in dural sinuses is usually of slightly increased density relative to brain parenchyma and especially near the torcula herophili.

Question 22

What is a “cashew nut sign”?

Answer 22

Its a less than 20mm concave shaped ICH in the juxtacortical area, often near the bottom of a cortical sulcus. 98% SPECIFICITY for ICH due to venous thrombosis, typically of SSS. But not sensitive (26%)

Question 23

Define vasogenic edema

Answer 23

• The BBB is disrupted.
• The edema is extracellularly and mainly affect the white matter via leakage of fluid from capillaries.

Question 24

Where is vasogenic cerebral edema mostly seen?

Answer 24

• MOST frequent around brain tumors, (primary and secondary tumors).
• Cerebral abscesses
  BUT ALSO:
• cerebral contusions
• cerebral hemorrhage
  IF BILATERAL and widespread:
• PRES

Question 25

How is vasogenic edema seen on CT?

Answer 25

• grey-white matter differentiation INTACT
• Edema involves mainly white matter - extending in finger-like fashion.

SECONDARY EFFECTS:
*Effacement (utplåning) of cerebral sulci w or w/o midline shift.

Question 26

How is vasogenic edema seen om MRI?

Answer 26

HYPERINTENSE T2 and FLAIR which DOES NOT show restricted diffusion.

Question 27

Define cytotoxic edema

Answer 27

Extracellular water passes into cells, resulting into their swelling. = cellular edema

Question 28

How is cytotoxic cerebral edema usually used in clinical practice?

Answer 28

To denote a combination of true cytotoxic edema and ionic cerebral edema.

Question 29

Explain the pathophysiology of cytotoxic edema

Answer 29

Inability of cells to maintain ATP-dependent Na/K membrane pumps that normally are responsable for high extracellular and low intracellular Na conc.
Na accumulate in the cells.
Osmotic gradiant created draw Cl and H2O into the cells that swell and the extracellular volume is reduced.

Question 30

How is the pathology of cytotoxic brain edema seen on MRI?

Answer 30

As restriced diffusion.

Question 31

How is restricted diffusion seen on MRI?

Answer 31

Its seen by high signal on DWI and low ob ADC. (T1WI and T2WI may only detect an infarct after about 6 hours)

Question 32

What type of brain cells are affected by cytotoxic edema?

Answer 32

Mainly the grey matter but also astrocytes in the white matter.

Question 33

How is the endothel affected by cytotoxic edema?

Answer 33

It is not involved, the BBB is therefore not compromised and no change in capillary permeability is seen.

Question 34

How is cytotoxic edema seen on CT? What important clinical fact does that explain?

Answer 34

It is NOT seen as mere redistribution of water from extracellular to intracellular compartments does not result in attenuation changes.

THIS IS WHY BRAIN CT IS NORMAL IN A PATIENT W ACUTE ISCHEMIC STROKE.

Question 35

What is the only sequense on MRI that is able to detect cytotoxic edema?

Answer 35

DWI ! - Diffusion weighted imaging.
-the commensurate decrease in diffusion is identified as high signal in DWI and low on ADC.

Question 36

How long does the initial changes in DWI and ADC persist after acute brain ischemia?

Answer 36

Into the subacute phase about two weeks after.

Question 37

Does steroids have a place in treatment of cytotoxic edema?

Answer 37

NO. Its not beneficial after stroke and may be HARMFUL in cytotoxic edema from TRAUMA.

Question 38

What is ionic edema?

Answer 38

It represents the passage of water and sodium from capillaries into the brain parenchymal EXTRACELLULAR space. The BBB remains INTACT.
It is usually associated to cytotoxic edema.

Question 39

Is ionic edema used in praxis?

Answer 39

no. It is usually combined with and denoted as cytotoxic edema (cellular swelling).

Question 40

Pathology behind ionic edema?

Answer 40

When cytotoxic edema draw H2O and Na into the cell, the ECM lack these components, and if there is still bloodflow in capillaries, a second gradient, now from capillary to ECM will form. Sodium along a electrochemical gradient and with it Cl AND H2O therewith osmotically. A secondary TISSUE SWELLING will occur.

Question 41

What type of edema is responsible for tissue swelling after stroke?

Answer 41

Ionic edema. (Na gradient created brings H2O into the ECM.