| Cerebral circulation | |
|---|---|
 Areas of the brain are supplied by different arteries. The major systems are divided into an anterior circulation (theanterior cerebral artery andmiddle cerebral artery) and a posterior circulation. | |
 Schematic of veins and venous spaces that drain deoxygenated blood from the brain | |
| Identifiers | |
| MeSH | D002560 |
| Anatomical terminology | |
Cerebral circulation is the movement ofblood through a network ofcerebral arteries andveins supplying thebrain. The rate of cerebralblood flow in an adulthuman is typically 750milliliters perminute, or about 15% ofcardiac output.Arteries deliveroxygenated blood,glucose and other nutrients to the brain.Veins carry "used or spent" blood back to theheart, to removecarbon dioxide,lactic acid, and othermetabolic products. Theneurovascular unit regulates cerebral blood flow so that activated neurons can be supplied with energy in the right amount and at the right time.[1] Because thebrain would quickly suffer damage from any stoppage in blood supply, the cerebral circulatory system has safeguards includingautoregulation of theblood vessels. The failure of these safeguards may result in astroke. Thevolume of blood in circulation is called thecerebral blood flow. Sudden intense accelerations change thegravitational forces perceived by bodies and can severelyimpair cerebral circulation and normal functions to the point of becoming serious life-threatening conditions.
The following description is based on idealized human cerebral circulation. The pattern of circulation and itsnomenclature vary between organisms.
Blood supply to the brain is normally divided into anterior and posterior segments, relating to the different arteries that supply the brain. The two main pairs of arteries are theinternal carotid arteries (supply the anterior brain) andvertebral arteries (supplying thebrainstem and posterior brain).[2] The anterior and posterior cerebral circulations are interconnected via bilateralposterior communicating arteries. They are part of thecircle of Willis, which provides backup circulation to the brain. In case one of the supply arteries is occluded, the circle of Willis provides interconnections between the anterior and the posterior cerebral circulation along the floor of the cerebral vault, providing blood to tissues that would otherwise becomeischemic.[3]
Theanterior cerebral circulation is the blood supply to the anterior portion of the brain includingeyes. It is supplied by the following arteries:
Theposterior cerebral circulation is the blood supply to the posterior portion of the brain, including theoccipital lobes,cerebellum andbrainstem.It is supplied by the following arteries:
The venous drainage of the cerebrum can be separated into two subdivisions: superficial and deep.
The superficial system is composed ofdural venous sinuses,sinuses (channels) within thedura mater. The dural sinuses are therefore located on the surface of the cerebrum. The most prominent of these sinuses is thesuperior sagittal sinus which is located in the sagittal plane under the midline of the cerebral vault, posteriorly and inferiorly to theconfluence of sinuses, where the superficial drainage joins with the sinus that primarily drains the deep venous system. From here, twotransverse sinuses bifurcate and travel laterally and inferiorly in an S-shaped curve that forms thesigmoid sinuses which go on to form the twojugular veins. In the neck, thejugular veins parallel the upward course of thecarotid arteries and drain blood into thesuperior vena cava. The veins puncture the relevant dural sinus, piercing the arachnoid and dura mater asbridging veins that drain their contents into the sinus.[5]
The deep venous system is primarily composed of traditionalveins inside the deep structures of the brain, which join behind the midbrain to form thegreat cerebral vein (vein of Galen). This vein merges with theinferior sagittal sinus to form thestraight sinus which then joins the superficial venous system mentioned above at theconfluence of sinuses.
The maturation of blood vessels in the brain is acritical process that occurs postnatally.[6] It involves the acquisition of key barrier and contractile properties essential for brain function. During the early postnatal phase,endothelial cells (ECs) andvascular smooth muscle cells (VSMCs) undergo significant molecular and functional changes.
Endothelial cells begin to expressP-glycoprotein, a crucialefflux transporter that helps protect the brain by expelling harmful substances.[7] This efflux capacity is progressively acquired and becomes fully functional by the postnatal period. Additionally, VSMCs, which initially populate the arterial network, start to express contractile proteins such as smooth muscleactin (SMA) andmyosin-11, transforming VSMCs into contractile cells capable of regulating blood vessel tone and cerebral blood flow.
The expression of Myh11 in VSMCs acts as a developmental switch, with significant upregulation occurring from birth to the age of 2 to 5 years.[6] This is a critical period needed for the establishment of vessel contractility and the overall functionality of the cerebral circulation.
Cerebral blood flow (CBF) is the blood supply to thebrain in a given period of time.[8] In an adult, CBF is typically 750 millilitres per minute or 15.8 ± 5.7% of thecardiac output.[9] This equates to an averageperfusion of 50 to 54 millilitres of blood per 100 grams of brain tissue per minute.[10][11][12]
The ratio index of cerebral blood flow/cardiac output (CCRI) decreases by 1.3% per decade, even though cardiac output remains unchanged.[9] Across the adult lifespan, women have a higher CCRI than men.[9] CBF is inversely associated withbody mass index.[9]
CBF is tightly regulated to meet the brain'smetabolic demands.[10][13] Too much blood (a clinical condition of a normal homeostatic response ofhyperemia)[1] can raiseintracranial pressure (ICP), which can compress and damage delicate brain tissue. Too little blood flow (ischemia) results if blood flow to the brain is below 18 to 20 ml per 100 g per minute, and tissue death occurs if flow dips below 8 to 10 ml per 100 g per minute. In brain tissue, abiochemical cascade known as theischemic cascade is triggered when the tissue becomes ischemic, potentially resulting in damage to and the death ofbrain cells. Medical professionals must take steps to maintain proper CBF in patients who have conditions likeshock,stroke,cerebral edema, andtraumatic brain injury.
Cerebral blood flow is determined by a number of factors, such asviscosity of blood, how dilatedblood vessels are, and the net pressure of the flow of blood into the brain, known ascerebral perfusion pressure, which is determined by the body'sblood pressure. Cerebral perfusion pressure (CPP) is defined as the mean arterial pressure (MAP) minus the intracranial pressure (ICP). In normal individuals, it should be above 50 mm Hg. Intracranial pressure should not be above 15 mm Hg (ICP of 20 mm Hg is considered as intracranial hypertension).[14] Cerebral blood vessels are able to change the flow of blood through them by altering their diameters in a process calledcerebral autoregulation; they constrict when systemic blood pressure is raised and dilate when it is lowered.[15] Arterioles also constrict and dilate in response to different chemical concentrations. For example, they dilate in response to higher levels ofcarbon dioxide in the blood and constrict in response to lower levels of carbon dioxide.[15]
For example, assuming a person with an arterial partial pressure of carbon dioxide (PaCO2) of 40 mmHg (normal range of 38–42 mmHg)[16] and a CBF of 50 ml per 100g per min. If the PaCO2 dips to 30 mmHg, this represents a 10 mmHg decrease from the initial value of PaCO2. Consequently, the CBF decreases by 1ml per 100g per min for each 1mmHg decrease in PaCO2, resulting in a new CBF of 40ml per 100g of brain tissue per minute. In fact, for each 1 mmHg increase or decrease in PaCO2, between the range of 20–60 mmHg, there is a corresponding CBF change in the same direction of approximately 1–2 ml/100g/min, or 2–5% of the CBF value.[17] This is why small alterations in respiration pattern can cause significant changes in global CBF, specially through PaCO2 variations.[17]
CBF is equal to thecerebral perfusion pressure (CPP) divided by the cerebrovascular resistance (CVR):[18]
Control of CBF is considered in terms of the factors affecting CPP and the factors affecting CVR. CVR is controlled by four major mechanisms:
Increasedintracranial pressure (ICP) causes decreased blood perfusion ofbrain cells by mainly two mechanisms:
Cerebral perfusion pressure is the netpressure gradient causingcerebral blood flow to the brain (brainperfusion). It must be maintained within narrow limits; too little pressure could cause brain tissue to becomeischemic (having inadequate blood flow), and too much could raiseintracranial pressure.
Arterial spin labeling (ASL),phase contrast magnetic resonance imaging (PC-MRI), andpositron emission tomography (PET) areneuroimaging techniques that can be used to measure CBF. ASL and PET can also be used to measure regional CBF (rCBF) within a specific brain region.rCBF at one location can be measured over time bythermal diffusion[19]