Table of Contents
- Cerebral Vasculature
- Autoregulation of Cerebral Blood Flow
- Myogenic Control of Cerebral Blood Flow
- Metabolic Control of Cerebral Blood Flow
- Neurogenic Control of Cerebral Blood Flow
- Neurovascular Coupling
- Table 1: Different Physiological and Pathological conditions and their association with CBF auto-regulation
- Effect of Blood Gas Levels and Temperature
- Measurement of Cerebral Blood Flow
- Table 2: Common methods of cerebral blood flow measurement along with their features and limitations
- Further Readings
- Brain tissue has high metabolic demand and high neuronal activity requires functional hyperemia for supply of nutrients and Oxygen
- 20% of total body oxygen and 25% of glucose utilization is dedicated to brain
- Various autoregulatory mechanisms and local and neuronal factors work together to ensure adequate brain perfusion
- Cerebral blood flow is defined as the volume of arterial blood delivered to a unit mass of brain tissue per unit of time.
- It is described in ml of blood per 100 gram of brain tissue per minute.
- The normal value is 50 ml/100g/min
- White matter has relatively lower CBF i.e. 20 ml/100g/min
- The grey matter has relatively higher CBF i.e. 80 ml/100g/min
- A highly complex interconnected network of vessels
- Feeding vessels include:
- Right and left internal carotid arteries anteriorly (~70 %)
- Right and left vertebral arteries posteriorly
- Vertebral arteries join to form the basilar artery
- Internal carotid and basilar artery are linked by the circle of Willis
- Circle of Willis connects these vessels on the inferior surface of the brain and consists of:
- Right and left anterior cerebral arteries (Branches of Internal Carotid Arteries)
- Anterior and posterior communicating arteries
- Middle cerebral arteries are also connected to the circle of Willis
- The flow of blood through the brain can be described by Ohm’s law:
Q = △P/R
- This indicates:
- The direct relation between pressure difference and cerebral blood flow.
- Increase in pressure difference ➨ Increase in cerebral blood flow
- Decrease in resistance ➨ increase in cerebral blood flow
- Resistance of vessel is determined by the radius of vessel, length of the vessel, and hematocrit i.e viscosity (Poiseuille’s law)
- Cerebral blood flow is mainly determined by change in vessel radius especially in small vessels i.e arterioles
- To maintain adequate cerebral blood flow, a decrease in blood pressure will require an increase in vessel radius (opposite to normal vessel response).
Autoregulation of Cerebral Blood Flow
- Cerebral perfusion pressure (CPP) and cerebrovascular resistance (CVR) are main factors that control Cerebral blood flow.
- Changes in CPP can be due to physiological (exercise) or pathological (TBI) processes.
- During cerebral autoregulation, optimal perfusion pressure is maintained by changes in CVR.
- Cerebral blood flow is kept relatively constant through the change in vessel diameter at the CPP range of 40-140 mmHg.
- CBF is regulated by the change in vessel radius between 50-150 mmHg MAP
- Cerebral autoregulation acts as a negative feedback mechanism to control the effect of increased MAP on CPP and keep CPP constant by reducing the radius of vessels when MAP is raised and vice versa.
- Static cerebral autoregulation ➨ CBF and MAP changes under steady-state conditions (minutes or hours)
- Dynamic cerebral autoregulation ➨ Transient changes in CBF and MAP and CBF (in seconds)
- The change in radius of vessels is the single most important factor in CBF autoregulation.
- Increased hematocrit ➨ increased viscosity ➨ low CBF
- Decreased hematocrit ➨ decreased viscosity ➨ increase CBF
- CBF is controlled by means of myogenic, metabolic, and neurogenic factors and partial pressure of arterial blood gases (CO2 and O2), cerebral metabolism, and the autonomic nervous system are primary determinants of CBF.
Myogenic Control of Cerebral Blood Flow
- The myogenic mechanism is the response of small arteries to intravascular pressure changes
- Arterial membrane depolarization results in the influx of Ca2+ in the arterial wall through voltage-dependent Ca2+ channels.
- It is a fast process mediated by EDRF and NO and occurs within 1-10 sec of change in pressure.
Metabolic Control of Cerebral Blood Flow
- Metabolic response alteration in blood flow secondary to blood pressure changes
- Changes in diameter of cerebral vasculature in response to alterations in the concentration of vasodilator metabolites like adenosine
Neurogenic Control of Cerebral Blood Flow
- The neurogenic response consists of perivascular neurons that autoregulate the cerebral blood flow by gliovascular interactions and intramural vascular signaling.
- Astrocytes act as mediators for signaling from neurons to the cerebral vasculature.
- Extrinsic nerves from peripheral nerve ganglia control surface vessels (Pial arteries) and large arteries (ICA, VA, MCA) whereas intrinsic nerves from intrinsic brain neurons control vessels within the brain parenchyma which has high basal tone and respond less to neurotransmitters.
- The vessel tone of large arteries is maintained by:
- Sympathetic neurons ➨ Superior cervical ganglion ➨ Norepinephrine, Neuropeptide Y
- Parasympathetic neurons ➨ Otic and Pterygopalatine ganglion ➨ Acetylcholine, VIP, NO
- Capillary dilation is faster than arteriolar dilation and is assumed to be caused by the active relaxation of pericytes.
- Veins contain 3/4th of cerebral blood volume but contribute less to autoregulation due to their less baseline tone.
- CBF is increased to accommodate greater metabolic demands of the brain via the process of neurovascular coupling.
- Neurovascular coupling is a temporal and regional linkage between neuronal activity and blood supply to the brain and is mediated by a number of metabolic by-products (lactate, adenosine), neurotransmitters (dopamine, acetylcholine), and vasoactive mediators (Ca2+, H+).
- Uncoupling due to any pathologic process results in loss of normal functioning of brain processes
Table 1: Different Physiological and Pathological conditions and their association with CBF auto-regulation
Effect of Blood Gas Levels and Temperature
- Increased arterial CO₂ dilates the cerebral vessels by changing extracellular pH and thus increasing blood flow.
- 1 mmHg increase in arterial PaCO₂ leads to 3-6 % elevation in CBF whereas 1 mmHg decrease in PaCO₂ reduce the CBF by 1-3%
- Hypoxia below 50 mmHg is potent vasodilator and thus increases cerebral blood flow.
- Cerebral metabolic rate decreases with hypothermia. 1 degree Celsius decrease in temperature reduces cerebral metabolic rate by 6-7 % and CBF decreases proportionately.
Measurement of Cerebral Blood Flow
- The direct methods measure the delivery of arterial blood to the capillary bed and measure the amount of tracer delivered to brain tissue by blood flow.
- Most of the methods use exogenous or endogenous compounds whose passage is taken as an indicator of cerebral blood flow. These methods rely on Fick Principle.
- Indirect methods measure cerebral perfusion indirectly and do not quantify the direct measure of blood delivered to brain tissue.
Table 2: Common methods of cerebral blood flow measurement along with their features and limitations
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CSO at NeuroCare.AI, Postdoctoral Intern at Global Innervation, Anne Rowling Clinic Regenerative Neurology Scholar
Founder NeuroCare.AI, Practicing Neurologist, sub-specialized in the field of Neurocritical Care, Stroke & Epilepsy