CSF Flow Anatomy Flashcards

1
Q

What does the carotid canal receive?

A

the internal carotid artery from the neck

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2
Q

Where does the carotid canal lie?

A

in the pyramid-shaped PETROUS part of the temporal bone

edges of carotid canal are smooth and rounded

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3
Q

What is the difference between ‘lacerated’ and ‘incised’?

A

lacerated = torn (with blunt force)

incised = cut (with sharp object)

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4
Q

Why might damage to the wall of the internal carotid artery cause Horner’s syndrome?

A

damage to the internal carotid (sympathetic) plexus

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5
Q

Why might an internal carotid aneurysm cause lateral rectus palsy?

A

the abducens nerve (CN VI) travels forward in the cavernous sinus with the internal carotid artery (ICA)

(other nerves travel in the lateral wall)

Abducens is therefore more vulnerable to compression due to ICA aneurysm

this can cause denervation of the ipsilateral lateral rectus muscle
=> diplopia, worse on far LATERAL GAZE of affected eye

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6
Q

What proportion of blood flow does the middle cerebral artery receive?

A

receives 80% of the internal carotid blood flow

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7
Q

What do the branches of the middle cerebral artery supply?

A

UPPER DIVISION
supplies frontal and parietal lobes

LOWER DIVISION
passes downwards to supply the temporal lobe

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8
Q

Why might a middle cerebral artery stroke cause paralysis of the contralateral face and upper limb but spare the lower limb?

A

the leg (lower limb) area of the primary motor cortex gives rise to the corticospinal cord

this is located MEDIALLY (paracentral lobule)
supplied by the anterior cerebral artery (ACA)

Areas for ‘arm’ (upper limb) and ‘face’ (cranial nerve/bulbar fibres) are supplied by the middle cerebral artery (MCA)
Area originates in the cerebral convexity

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9
Q

What is the most likely cause of a stroke affecting the middle cerebral artery territory?

A

most strokes are ischaemic (85%) rather than haemorrhagic (15%)

Ischaemic strokes are most commonly caused by an EMBOLUS coming from the heart or atherosclerotic neck vessels

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10
Q

What is the mechanism of AF increasing stroke risk?

A

AF = atrial fibrillation

mural thrombus originates from the left atrial appendage (blood sits and can easily form clots)

common cause of stroke

especially since 10% over the age of 75 have AF

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11
Q

What is the mechanism for clot formation in coronary circulation?

A

myocardial infarcts are also occlusive in origin

but most commonly caused by IN SITU THROMBUS
e.g. due to unstable atherosclerotic plaque then vascular occlusion from the displaced thrombus and downstream MI

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12
Q

What is the smaller branch off of the internal carotid that passes superiorly and medially into the longitudinal fissure?

A

anterior cerebral artery

receives 20% of the blood from the internal carotid blood flow

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13
Q

Where is the ACA in relation to the optic chiasm?

A

ACA = anterior cerebral artery

ACA sits above the optic chiasm

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14
Q

What is the point where the 2 anterior cerebral arteries connect called?

A

the anterior communicating artery

part of the circle of Willis

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15
Q

What is the branch of the ACA that winds around the corpus callosum?

A

pericallosal branch of the ACA

[other branches fan out over the medial surface of the hemisphere]

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16
Q

What does the ACA supply?

A

medial surface of the brain as far back as the deep parieto-occipital sulcus

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17
Q

What supplies the brain posterior to the deep parieto-occipital sulcus?

A

posterior cerebral artery (PCA)

supplies the posterior region = medial surface of the occipital lobe

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18
Q

Why might an anterior cerebral artery (ACA) stroke cause paralysis of the contralateral lower limb but spare the upper limb and face?

A

ACA supplies medial part of the motor strip (paracentral lobule)
this contains the primary motor cortex (controls contralateral lower extremity)

upper limb and facial areas of motor cortex supplied by MCA

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19
Q

Would you expect an anterior cerebral artery (ACA) stroke to cause a contralateral visual field defect (hemianopia)?

A

No
ACA does not supply the visual cortex or the central visual pathways from the lateral geniculate nucleus to the calcarine sulcus

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20
Q

Why might a MCA stoke cause a visual field defect?

A

can interrupt the optic radiations as they sweep down through the temporal and up through the parietal lobes to reach the visual cortex

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21
Q

Would an embolus travelling up the internal carotid artery be more likely to enter the ACA or MCA?

A

~80% of the ICA blood flows laterally into the MCA (bigger diameter)

other 20% flow passes anteriorly and medially to enter the ACA

therefore more likely for embolus to enter the MCA

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22
Q

Where do the paired vertebral arteries arise from?

A

subclavian arteries in the neck

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23
Q

Where do the vertebral arteries pass in the cervical vertebrae?

A

pass through the upper 6 cervical transverse foramina

not C7

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24
Q

What is the course of the vertebral arteries?

A

ascend the cervical vertebra roughly parallel to the carotid vessels

enter skull via the foramen magnum

they then unite to form the basilar artery

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25
Q

Why might a violent flexion-extension neck injury to the neck lead to a brain stem stroke?

A

by tearing/damaging the vertebral artery lining as it passes through the foramina transversaria to ascend the neck

may trigger local vessel thrombosis -> occlusion -? could cut off posterior circulation supply

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26
Q

What is the medical term for a tear in an arterial wall?

A

arterial dissection

DISS-SECTION not DIE-SEKSHUN

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27
Q

In what age group is arterial dissection more common?

A

more likely to occur in a younger patient <50

in those who lack the usual risk factors for stroke

however, arterial dissections are generally unusual

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28
Q

When may vertebral arteries be absent?

A

if brain stem transection is high

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29
Q

Where does the basilar artery ascend?

A

in the basilar groove of the pons

30
Q

In life, where does the basilar artery lie?

A

rests on the sloping base of the skull (known at the CLIVUS)

31
Q

Where is the terminal bifurcation of the basilar artery?

A

at the upper border of the pons

here it divides into the 2x posterior cerebral arteries (PCA)

32
Q

Where do the posterior cerebral arteries travel?

A

wind around the midbrain

supply the inferior surfaces of the cerebral hemispheres

also supply the medial surface of the occipital lobe

33
Q

Where do the posterior communicating arteries pass?

A

between the internal carotid artery and posterior cerebral artery on each side

(these vessels will form part of the circle of Willis)

34
Q

Why is thrombosis of the entire basilar artery likely to be fatal?

A

loss of brain stem blood supply

will interfere with the vital cardiorespiratory centres

35
Q

What visual field defect would you expect with occlusion of the distal basilar artery?

A

If a saddle embolus/thrombus lodges in the crotch of the distal basilar artery where it bifurcates

this can cut off the entire blood supply to both posterior cerebral vessels

=> ischaemia of both occipital lobes
=> total occipital infarction
=> cortical blindness

however, if one/both posterior communicating arteries is large, then it may compensate by receiving retrograde flow from the ICA
(perfusion of occipital cortex)

36
Q

Where does the superior cerebellar artery (SCA) reside?

A

superior cerebellar artery (SCA) sits immediately below the posterior cerebral artery (PCA)

37
Q

Which cranial nerve emerges between the SCA and PCA?

A

oculomotor nerve (CN III)

SCA = superior cerebellar artery

PCA = posterior cerebral artery

38
Q

Where doe the anterior inferior cerebellar artery (AICA) arise from?

A

usually from the lower part of the basilar artery

39
Q

Where does the posterior inferior cerebellar artery (PICA) usually arise from?

A

from the vertebral artery on each side

40
Q

What clinical features would you expect following a large cerebellar haemorrhage?

A

usually cerebellar features e.g. ataxia on ipsilateral side

also, space-occupying effect of haematoma (plus oedema + swelling) would cause increased ICP

likely to be exacerbated by compression of the 4th ventricle, leading to outflow obstruction and acute hydrocephalus

41
Q

If a haemorrhage affected the left cerebellar hemisphere, on which side of the body would you expect to see clinical signs?

A

Ipsilateral (left)

cerebellar hemispheres are “uncrossed”

42
Q

Why might left cerebellar hemisphere haemorrhage be an emergency?

A

posterior fossa mass
=> swelling/oedema
=> secondary acute hydrocephalus

=> may lead to tonsilar herniation
=> respiratory depression/death

emergency surgical evacuation of the haematoma may therefore be required

43
Q

Where does the blood supply to the brain stem arise?

A

from the posterior circulation

44
Q

What kind of vessels are the cerebellar arteries?

A

long circumferential arteries

SCA
AICA
PICA

45
Q

Why might occlusion of the pontine paramedian arteries cause paralysis of all 4 limbs from the neck down (quadriplegia)?

A

destruction of the corticospinal (pyramidal) tracts

these descend in the basal/anterior pons

corticobulbar innervation to the lower cranial nerves (e.g. tongue, lateral rectus) would probably also be affected

46
Q

Why kind of eye movements may be spared/affected in an infarction of the pontine paramedian arteries? What is this clinical picture known as?

A

VERTICAL EYE MOVEMENTS

  • vertical gaze centre in in the midbrain
  • its corticobulbar innervation has already reached its target about the level of the lesion (basal pons)

LATERAL EYE MOVEMENTS

  • likely to be affected
  • lateral gaze centre and nucleus of the abducens (CN VI) nerve is in the pons

Clinical picture: Locked-in syndrome

47
Q

What supplies the deep grey area of the brain?

A

central perforating vessels

48
Q

Where do the lenticulo-striate arteries arise from?

A

middle cerebral artery

49
Q

What are the boundaries between the 3 arterial territories known as?

A

arterial watersheds

50
Q

What is the ‘triple watershed area’ of the brain?

A

most vulnerable region for where ACA, MCA and PCA converge in the parieto-occipital region

posterior to the lateral ventricles

51
Q

Why might cardiac arrest lead to a stroke at the boundary zone between the territories of 2 major cerebral arteries (watershed infarct)?

A

profound arterial hypotension and relative low pressure/perfusion during resuscitation

core vascular territories might just be adequately perfused, but the peripheries of vascular territories and regions between 2 supplies will receive the least blood at the lowest pressure

=> critical ischaemia and infarction
=> “watershed” areas

52
Q

Why might someone suffer a watershed infarct after being stung by a wasp?

A

anaphylactic shock

53
Q

Which vascular territories would be affected by a complete occlusion of the left internal carotid artery?

A

Middle cerebral artery (MCA) and anterior cerebral artery (ACA) territories arise from the ICA

ICA occlusion -> total anterior circulation syndrome (TACS)
this carries a >60% risk of death

54
Q

What are the dural venous sinuses?

A

valveless spaces between 2 layers of dura lined by endothelium

occur at the free and attached margins of the dural folds

55
Q

Where is the superior saggital sinus?

A

in the attached margin of the FALX CEREBRI

major sinus: receives blood from the superior surfaces of the hemispheres

56
Q

Where is the inferior saggital sinus located?

A

in the free margin of the FALX
drains into the straight sinus (between falx and tentorium cerebelli)

straight sinus receives blood from deep cerebral veins

57
Q

Where are the transverse sinuses?

A

in the attached margins of the tentorium cerebelli

58
Q

Where does the superior saggital sinus drain?

A

into the RIGHT TRANSVERSE SINUS

59
Q

Where does the straight sinus drain?

A

into the LEFT TRANSVERSE SINUS

60
Q

Where do the transverse sinuses drain?

A

they become the S-shaped sigmoid sinuses

which then discharge into the bulb of the internal jugular vein on each side

61
Q

Why might thrombosis of the superior saggital sinus cause extensive haemorrhage over the surface of both cerebral hemispheres?

A

failure to drain superficial cerebral veins

leads to over-filling, confession and increasing back-pressure in the superficial cerebral venous bed

may ultimately lead to rupture with extensive superficial venous haemorrhage over both cerebral hemispheres

62
Q

What are the main risk factors for venous sinus thrombosis?

A
  • dehydration
  • malignancy
  • infection
  • pregnancy
  • OCP
  • clotting abnormalities (e.g. factor V Leiden etc)
63
Q

Why might meningioma be very difficult to remove surgically if it is close to/surrounding a major venous sinus?

A

it is liable to bleed

like a stuck pig

64
Q

What is a meningioma?

A

a benign tumour that arises from the meninges

65
Q

Where are the arachnoid granulations located?

A

on either side the longitudinal fissure

will correspond to an arachnoid villous projecting into the superior saggital sinus

66
Q

Where is the CSF absorbed into the ventricular system?

A

at the point at which arachnoid villi project into the superior saggital sinus

67
Q

Where is CSF produced?

A

in highly vascular choroid plexuses

68
Q

What are the main structural horns of the lateral ventricle?

A
  • frontal
  • temporal
  • occipital
69
Q

Where is the cerebral aqueduct?

A

between the third and fourth ventricles

70
Q

Where in the interventricular foramina?

A

[Foramina of Monro]

located between the lateral and third ventricles

71
Q

How many openings for CSF are there in the fourth ventricle?

A

3 openings:
1 medial: FORAMEN OF MAGENDIE
2 lateral: FORMANINA OF LUSHKA

4th ventricle is diamond shaped btw

72
Q

What would happen if the foramina in the 4th ventricle were occluded?

A

this would block outflow from the ventricular system

CSF would be continually produced by choroid plexuses with no means of escape

=> dilation of entire ventricular system
=> raised ICP
=> papilloedema (optic disc swelling)
=> acute hydrocephalus (sharp increase in ICP)
=> tonsillar herniation and death

can be managed neurosurgically: insertion of external ventricular drain or ventriculoperitoneal (VP) shunt