Pial arteries form a network of small vessels covering the surface of the brain, delivering oxygenated blood directly to the brain tissue. These arteries are the final conduits in the vascular system that supports the high metabolic demands of nerve cells. The health of this arterial network is directly linked to proper brain function, as any disruption in the system can have significant consequences.
Anatomy of the Pial Arterial Network
The brain is enveloped by three protective membranes called the meninges. The innermost layer is the pia mater, a thin membrane that adheres closely to the brain’s surface, following every contour. The pial arterial network is situated on this layer within the subarachnoid space, which separates the pia mater from the arachnoid mater. This space is filled with cerebrospinal fluid, providing a cushion for the brain and its vascular network.
This network of vessels originates from the larger anterior, middle, and posterior cerebral arteries. As these major arteries branch, they form the smaller pial arteries that spread across the cortical surface. These surface vessels create an interconnected system, or plexus, ensuring some redundancy in the blood supply. The network is composed of arteries and arterioles with diameters ranging from 50 to 280 micrometers.
From this surface network, smaller penetrating arteries diverge at nearly right angles, moving perpendicularly into the cerebral cortex. This arrangement allows blood to transition from the superficial network into the brain tissue to nourish the underlying neurons. The pial arteries and their penetrating branches are the primary source of blood for the brain’s neocortex.
Role in Supplying the Cerebral Cortex
The primary function of the pial arterial network is distributing oxygenated blood to the neurons of the cerebral cortex. This outer layer of the brain is responsible for higher cognitive functions like thought, language, and memory. The high energy requirements of cortical neurons necessitate a precisely regulated blood supply, which the pial arteries provide.
A main function of these vessels is cerebral autoregulation, the ability to maintain stable blood flow despite fluctuations in systemic blood pressure. Pial arteries and arterioles actively adjust their diameter by constricting when blood pressure rises and dilating when it falls. This response ensures neurons receive a consistent blood supply, protecting them from insufficient flow or excessive pressure.
The autoregulatory response is not uniform across the network. Smaller pial arterioles have a greater capacity to dilate during periods of low pressure compared to larger ones. As pressure increases, the smallest arterioles are the first to reach their maximum constriction. This multi-level response allows for precise adjustments that protect the brain’s microenvironment.
Conditions Affecting Pial Arteries
Several medical conditions can affect the pial arterial network. An ischemic stroke can occur if a pial artery is blocked by a thrombus (a locally formed clot) or an embolus (a clot from elsewhere). This blockage deprives a region of the cerebral cortex of oxygen, leading to tissue death and neurological deficits.
A subarachnoid hemorrhage is a stroke that occurs when a pial artery on the brain’s surface ruptures, causing blood to leak into the subarachnoid space. The presence of blood in this space increases pressure on the brain and can trigger inflammatory responses. This condition is often caused by a ruptured aneurysm, which is a balloon-like bulge in an artery’s wall.
Vascular malformations, like aneurysms or arteriovenous malformations (AVMs), can develop within the pial arterial network. An aneurysm is a weak spot in the vessel wall at high risk of rupturing. An AVM is a tangle of abnormal blood vessels creating a faulty connection between arteries and veins, bypassing the capillary system and increasing bleeding risk.
Following a subarachnoid hemorrhage, a complication called cerebral vasospasm can occur. This condition involves the prolonged narrowing of cerebral arteries, including pial arteries. Vasospasm is triggered by blood breakdown products in the subarachnoid space and begins 3 to 4 days after the hemorrhage, peaking around 7 to 10 days later. This constriction reduces blood flow, potentially causing delayed cerebral ischemia and further brain injury.