2.1 Cerebral Circulation Flashcards
Arterial Supply (Figure 2.1)
- The brain is supplied by four major vessels: two internal carotid arteries which
provide two-thirds of the arterial supply, and the two vertebral arteries which deliver
the remaining third. (Some texts quote an 80:20 distribution.) - The vertebral arteries give off the posterior inferior cerebellar arteries, before joining
to form the basilar artery. This also provides the anterior inferior cerebellar and the
superior cerebellar arteries. - The basilar artery then gives off the two posterior cerebral arteries, which supply the
medial side of the temporal lobe and the occipital lobe. - The artery then anastomoses with the carotid arteries via two posterior communicating
arteries. - The internal carotid arteries meanwhile give rise to the middle cerebral arteries which
supply the lateral parts of the cerebral hemispheres. They also provide much of the
supply to the internal capsule, through which pass a large number of cortical afferent
and efferent fibres. - The carotids also give rise to the anterior cerebral arteries, which are connected by
the anterior communicating artery and which supply the medial and superior aspects
of the hemispheres. - The three arterial stems (basilar and carotid arteries), linked by the anterior and
posterior communicating arteries, comprise the arterial circle of Willis.
This is said to be incomplete in up to 15% of normal asymptomatic subjects.
Venous System
- The cerebral and cerebellar cortices, which are relatively superficial structures, drain
into the dural sinuses.
These venous sinuses lie between the two layers of the cranial dura mater. The superior sagittal sinus lies along the attached edge of the falx cerebri,
dividing the hemispheres, and usually drains into the right transverse sinus. - The inferior sagittal sinus lies along the free edge of the falx and drains via the straight
sinus into the left transverse sinus. (The straight sinus lies in the tentorium cerebelli.)
The transverse sinuses merge into the sigmoid sinuses before emerging from the
cranium as the internal jugular veins. - Deeper cranial structures drain via the two internal cerebral veins, which join to form
the great cerebral vein (of Galen). This also drains into the inferior sagittal sinus.
4.The cavernous sinuses lie on either side of the pituitary fossa and drain eventually
into the transverse sinuses.
Supplementary and Clinical Information
Aneurysmal Subarachnoid Haemorrhage
Intracranial aneurysms account for about 85% of cases of spontaneous SAH;
the incidence is 1 in 10–12,000 persons per year.
The overall mortality rate approaches 50%, and morbidity amongst survivors is high.
Aneurysms are associated with a weakening of the tunica media
of the arterial wall and develop most commonly at vascular bifurcations.
Only 10–20% of aneurysms form in the posterior vertebrobasilar circulation.
Most are found in the anterior carotid circulation,
in the middle cerebral artery and in the anterior and posterior communicating arteries.
Initial aneurysm management
Initial management is as for any other acute cerebral injury,
with the emphasis on cardiorespiratory stabilization and
the prevention of secondary brain injury.
Treatment is either with endovascular occlusion using coils
or by aneurysm clipping via a direct neurosurgical approach.
The cumulative risk of rebleeding approaches 20% at 14 days.
Cerebral vasospasm:
this is the major cause of morbidity and mortality following SAH,
and occurs in up to 70% of cases.
It is a cause of delayed cerebral ischaemia (DCI).
Its peak onset is at 7–10 days,
may manifest as early as day 3 and usually resolves by 21 days.
There are various theories for its aetiology on which the oral
may touch, but their complexity precludes excessive detail.
Acutely there is an increase in intracellular calcium which0
follows exposure to haemoglobin and which produces contraction
(via phosphorylation of myosin light chains).
However, prolonged vasoconstriction is independent of intracellular calcium levels,
but it may be due to an increase in calcium responsiveness induced by endothelin.
DCI patho
Endothelin-1 (ET-1) is a potent vasoconstrictor
whose receptors are upregulated in response to cerebral ischaemia.
There is also a general increase in the density both of ET-1 and 5-HT1B receptors.
Other factors include the production of reactive oxygen species
and lipid peroxidation secondary to haemoglobin autoxidation
and changes in the scavenging or production of nitric oxide.
A large volume of subarachnoid blood (as seen on CT) is a
consistent predictor of the
development of vasospasm.
Prevention and management
: there is unlikely to be time to cover this in any detail,
so an understanding of the broad principles should suffice.
There is good evidence to support the prophylactic use
of the dihydropyridine calcium channel blocker nimodipine
which improves outcome
(typical dose regimen is 60 mg 4 hourly for 21 days).
Nimodipine blocks the slow calcium channel of vascular smooth muscle
and cardiac muscle but has no effect on skeletal muscle.
The British aneurysm trial demonstrated a 40% reduction in poor outcomes
(mortality and neurodisability).
Established or incipient cerebral vasospasm can be managed
with so-called triple-H therapy, or Hypertension, Hypervolaemia and Haemodilution
, the combination of which aims to increase perfusion pressure,
decrease blood viscosity and maximize cerebral blood flow.
While it is important to avoid hypotension, hypovolaemia and haemoconcentration,
triple-H therapy lacks evidence from controlled trials and its
use remains contentious.
A low haematocrit, for example, may improve cerebral blood flow but may reduce oxygen delivery
miscellaneous facts which may also prove useful
The circle of Willis provides effective collateral blood supply in the presence
of arterial occlusion.
Three out of four of the main arteries can be occluded as long as the process is gradual, without producing cerebral ischaemia. The normal intracranial blood volume is around 100–130 ml.
The middle cerebral artery has been described as ‘the artery of cerebral haemorrhage’.
This is mainly because it supplies the internal capsule, where a large number
of important cortical afferent and efferent fibres congregate.
The superficial areas of the cerebral (and cerebellar) cortex drain to the venous sinuses
via thin-walled veins.
These are vulnerable to rupture, with the formation of subdural
haematomas, particularly in the elderly in whom there is a loss of brain mass.
Other potential intracranial catastrophes
Other potential intracranial catastrophes include
cavernous sinus thrombosis,
sagittal sinus thrombosis and
cortical vein thrombosis (CVT).
CVT is particularly associated with pregnancy,
and is reported as occurring in between
1 in 3,000 and 1 in 6,000 deliveries.
If this figure is accurate, then CVT is being under-diagnosed,
because very few obstetric anaesthetists in an
average-sized maternity unit encounter
the one or two cases a year that this incidence would suggest.
It should always be
included in the differential diagnosis of peri-partum headache.
